Continuing Education
Depression and
Current Treatment
The
University of Mississippi School of Pharmacy is approved by
the
American Council on Pharmaceutical Education as a
provider of
continuing pharmaceutical education
This
program (# 032-000-03-062-H01) is
approved for 2 hours (0.2 CEU) of continuing pharmaceutical
education credit. A score of 70% on the examination is
required to receive CE credit.
This
lesson is no longer valid for CE credit after
12/31/2005
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Melanie Hammill Bishop, PharmD
King’s
Daughters
Medical
Center
Brookhaven
,
Mississippi
Needs Statement: Depression is a common and disabling disorder that is receiving increase recognition as a significant health problem. Pharmacists must be ready to recommended treatment options to health professionals. They must also be able to educate patients on current antidepressants.
Intended Audience: Pharmacists
Goal: To provide the pharmacist with an overview of depression with a focus on treatment.
Objectives:
Upon
successful completion of this lesson, the participant should
be able to:
1.
Discuss the signs and symptoms of depression
2.
Identify the medical conditions and medications that may cause
or worsen depression
3.
Compare and contrast the treatment options
4.
Explain the role of the CYP450 enzymes in prevention of drug
interactions
Introduction
Clinical depression affects some 26% of women and 13% of men
in the United
States. In
addition, the incidence is 2 to 3 times higher in first-degree
relatives of depressed
persons. Although
depression can occur at any age, adults 25 to 44 years of age
experience the highest
rates. Patients
with depression frequently develop other psychiatric
illnesses, such as anxiety disorders and
alcoholism.
Depression is the eighth leading cause of death in the United
States. Suicide
attempts by patients with major depression are severalfold
higher in comparison with the general
population.
Suicide by the depressed patient is not the only concern
regarding mortality in depressed
patients. Many
studies suggest that depressed patients with medical problems
have higher morbidity and
mortality. Results
of one study showed a 5-fold increased risk of death in
depressed patients over the 6 months following a myocardial
infarction (MI), and found that the impact of depression was
at least equivalent to that of left ventricular dysfunction
and a history of previous
MI. Outcomes are
also poor for poststroke patients with depression, as shown by
a study conducted in a consecutive series of 103 patients who
were assessed for major depression or dysthymia 2 weeks
following a stoke.
During the study’s 10-year follow-up period, depressed
patients were found to be 3.4 times as likely to die than
those without depressive symptoms.
Clinical Presentation/Diagnosis
When a patient presents with
depressive symptoms, it is necessary to investigate the
possibility of a medical, psychiatric, and/or drug induced
cause (Table
1). All
depressed patients should have a complete physical
examination, mental status examination, and basic laboratory
workup. To identify any potential medical problems, lab test
should include a complete blood count with differential,
thyroid function tests, and electrolyte
determinations.
Even though depression can be treated safely and effectively,
it remains underdiagnosed and
undertreated.
Major Depression can present as a single episode, but is often
recurrent and
chronic. It is
characterized by one or more major episodes consisting of a
period of at least 2 weeks in which the patient exhibits five
or more specific
symptoms. These
symptoms cause significant distress or impairment in social or
occupational functioning (Table
2). Symptoms must
not be due to the direct physiological effects of a substance
or a general medical condition, and they cannot be better
accounted for by bereavement. Severe depression can be
accompanied by psychotic
symptoms. A
simple way to remember the criteria for major depression is:
The prescription (SIG) for major depression is energy (E)
capsules (CAPS) - or SIG E CAPS.
Depressed patients must be assessed for suicidal
thoughts. Factors
that increase the risk of suicide include living alone,
substance abuse, family history of suicide, presence of a
serious medical condition, increasing age, unemployment,
divorce, death of a spouse, and prior
attempts. The
presence of a very detailed plan with the intention and
ability to carry it out indicates a high risk of suicide.
Pathogenesis
Many theories attempt to explain the pathophysiology of
depression. It is
likely that several different factors work together to cause
the illness.
Treatment that involves alterations in brain neurotransmitters
can improve symptoms and have provided clues to the
pathophysiology of
depression.
Primarily, serotonin and norepinephrine neurotransmitter
systems appear to play the greatest role in
depression. The
most widely accepted theory is that reduced levels of these
neurotransmitters lead to
depression. One
other theory states that decreased levels of serotonin may
allow for the expression of the mood disorder, but the level
of norepinephrine determines the type of disorder
displayed.
Another possible etiology is receptor upregulation, which
results from a decreased amount of neurotransmitter
chronically. There
are many other theories of cause including abnormal
neurokinins, decreased neurogenesis caused by heightened
glucocorticoid release, and structural and functional brain
changes.
General Overview of Treatment
Therapeutic options used in the treatment of depression are
psychotherapy, pharmacotherapy, and electroconvulsive therapy
(ECT). The
combination of psychotherapy and pharmacotherapy is the
optimal approach for most
patients. The
difficulty with psychotherapy is the fact that it is often
difficult to obtain, or not covered by third
parties.
Electroconvulsive
therapy (ECT) is very effective in treating refractory
depression.
Contrary to popular belief resulting from hearsay and movies
such as One Flew Over
the Cuckoo’s Nest, ECT is safe and
humane. The
patient is anesthetized and paralyzed and a nonconvulsive
seizure is induced for about 30
seconds. The
entire process takes about 1 to 2 hours in an outpatient
setting and the patient usually goes home after
treatment. A
course of ECT generally consists of
6 to
12
treatments
administered either unilaterally or bilaterally two to three
times weekly.
Contraindications to ECT include intracranial pressure,
cerebral lesions, recent myocardial infarction, recent
intracerebral hemorrhage, or
bleeding. The most
common side effect of ECT is short-term memory loss that tends
to improve with
time. Memory loss
is less pronounced with unilateral
ECT.
Recent advancement in the development of new and effective
antidepressants has been
astounding.
Studies comparing the efficacy of antidepressants have found
that they are of equivalent efficacy when administered in
comparable doses.
Factors that often influence the choice of an antidepressant
include the patient’s past history of response, familial
antidepressant response, the potential for drug-drug
interactions, adverse effects, and ability to target
particular depressive symptoms (i.e.
insomnia). One
would also want to avoid tricyclic antidepressants (TCAs) or
monoamine oxidase inhibitors (MAOIs) in patients who are
impulsive and at high risk for
overdose. Cost is
also a consideration in many patients; however, older
medications which are cheaper, have more side effects. The
mechanism of action of antidepressants is not
clear. It is
believed that adaptive changes in neurotransmission in the
brain occur with antidepressant
administration.
This process takes time to occur, and we generally inform
patients it will take 6 weeks to see antidepressant
effect. Anxiolytic
properties of antidepressants are manifested
sooner. Initially,
benzodiazepines are sometimes added for their benefit in
treatment of anxiety and
insomnia. If
depression is accompanied by psychosis, low dose antipsychotic
therapy is added to the antidepressant until those symptoms
resolve.
Although
definitive research is lacking, TCAs and SSRIs are used in the
treatment of childhood
depression. The
risk and benefits of antidepressant therapy in pregnancy must
be weighed, and concerns about the risks of untreated
depression during pregnancy should be
considered. No
major teratogenic effects have been identified with the SSRIs
or TCAs. Further
evaluation of antidepressants is needed to fully understand
the risk associated with their use.
Antidepressants will be placed into four basic categories for
discussion. These
are: tricyclic antidepressants (TCAs), monoamine oxidase
inhibitors (MAOIs), selective serotonin reuptake inhibitors
(SSRIs), and atypical antidepressants.
Tricyclic Antidepressants
(TCAs)
TCAs were among the first antidepressants
available.
Although effective, TCAs are considered as second or
third-line treatment due to their unfavorable side effect
profile and lethality potential when taken in
overdose. These
agents act by blocking the reuptake of serotonin and
norepinephrine.
The tertiary amines are frequently metabolized to secondary
amines that are active, and generally more potent for
norepinephrine
reuptake. The
activity of TCAs at other receptors, including cholinergic,
histaminergic, noradrenergic, and dopaminergic receptors,
leads to a broad spectrum of efficacy in disorders other than
depression, such as enuresis, chronic pain, and migraine
prophylaxis.
However, activity at these receptor sites also leads to the
unfavorable side effects such as dry mouth, urinary retention,
constipation, blurred vision, sedation, weight gain, and
sexual
dysfunction. These
drugs should be used with extreme caution in patients with
cardiac disease or seizure
disorders.
Patients at risk for orthostatic hypotension are at increase
risk of falls if they use these
agents.
Because TCAs are metabolized in the liver through the
cytochrome P450 system, they may interact with other drugs
that affect hepatic enzyme
activity. TCAs are
involved in pharmacodynamic drug interactions as
well. They may
reverse the hypotensive effects of certain antihypertensives
such as guanethidine, methyldopa, and
clonidine. TCAs
may increase the vasopressor response to phenylephrine and
epinephrine. Fatal
reactions may occur when combined with
MAOIs. Monitoring
of therapeutic serum concentration is beneficial when using
TCAs to confirm that the dose has led to a value within the
range for efficacy and to guard against toxic
values.
Monoamine Oxidase Inhibitors
(MAOIs)
MAOIs are effective antidepressants, but use of these agents
should be restricted to treatment-refractory depression or
atypical
depression. The
nonselective MAOIs inhibit type A and type B monoamine
oxidases, the enzymes responsible for the breakdown of
catecholamines such as norepinephrine, serotonin, and
dopamine. This enzyme blockade presumably results in an
increase in the concentration of these neurotransmitters in
neuronal synapses.
Common side effects include orthostatic hypotension, sedation,
dizziness, insomnia, constipation, tachycardia, peripheral
edema, sexual dysfunction, and weight
gain. Drug
interactions with the MAOIs are
significant.
Monoamine oxidases are also responsible for the breakdown of
certain amines found in foods, beverages, and OTC
sympathomimetics. Thus, combinations with many of these
substances can produce dangerous
interactions. If
MAOIs are used, thorough patient education and monitoring is
required so that patients avoid foods high in tyramine to
prevent a hypertensive crisis and subsequent
stroke.
Combination with other antidepressants can be problematic as
well. When
switching to or from another antidepressant, a washout period
is mandatory. The
MAOIs available in
the US are phenelzine and tranylcypromine.
Selective Serotonin Reuptake Inhibitors
(SSRIs)
Because of their comparable efficacy and better-tolerated
adverse effects, selective serotonin reuptake inhibitors
(SSRIs) have replaced tricyclic antidepressants as the drugs
of choice in the treatment of
depression. In
addition to depression, the SSRIs have proven efficacy in
treating anxiety disorders, including obsessive compulsive
disorder (OCD), panic disorder, social phobia, and post
traumatic stress disorder
(PTSD). SSRIs
block the reuptake of serotonin, therefore enhancing serotonin
activity within the
synapse. Although
this is the predominant mechanism of action of this class of
drugs, each SSRI has a slightly different pharmacological
profile that leads to its distinct clinical activity, side
effects, and drug interactions. It also appears that some
patients may respond to one but not another
SSRI.
The SSRIs have a low affinity for the histaminic, cholinergic,
and noradrenergic receptors and are generally well
tolerated. Common
side effects of SSRIs include transient nausea, diarrhea,
insomnia, somnolence, dizziness, akathisia, and long-term
sexual
dysfunction.
Because these drugs have such potent serotonergic activity,
combinations with other drugs affecting serotonin can lead to
serotonin
syndrome. Examples
include MAOIs, TCAs, dextromethorphan, and
meperidine.
Serotonin syndrome is manifested as confusion, hypomania,
restlessness, myoclonus, hyperreflexia, diaphoresis,
shivering, tremor, and
diarrhea.
Treatment of serotonin syndrome includes discontinuation of
the offending agents as well as supportive
measures. The
SSRIs are metabolized by the cytochrome p-450 system, leading
to interactions with drugs involved in that system (Table
3). As with
all antidepressants, care must be taken to screen patients for
symptoms of bipolar disorder before prescribing SSRIs, to
avoid precipitation of a manic
episode.
There are five SSRIs that are approved by the U.S. Food and
Drug Administration (FDA) for the treatment of depression,
which include fluoxetine (Prozac), sertraline (Zoloft),
paroxetine (Paxil), citalopram (Celexa), and escitalopram
(Lexapro).
Although fluvoxamine (Luvox) is an effective antidepressant,
it is only FDA approved for the treatment of OCD.
Fluoxetine (Prozac®):
Fluoxetine was the first SSRI to be FDA-approved for the
treatment of
depression.
Administration usually begins with 20mg per day, taken in the
morning because of its potential for central nervous system
activation. A
starting dose of 10mg per day is preferred in the elderly
patients.
Fluoxetine may be increased to 40 to 60mg for depression; 80mg
per day may be necessary for the treatment of
OCD. Fluoxetine
has a half-life of two to four days and its active metabolite,
norfluoxetine, has a half-life of seven to nine
days. The long
half –life makes fluoxetine beneficial in noncompliant
patients. It may
also be an appropriate antidepressant choice in patients with
hypersomnia or psychomotor
retardation.
Fluoxetine is now available in a special form taken
once-weekly for therapy of
depression. Prozac
Weekly is a capsule with pellets containing 90mg of fluoxetine
hydrochloride. The
enteric coating prevents dissolution of the pellets until they
have passed into the portion of the gastrointestinal tract
where the pH exceeds
5.5. In a study of
500 patients with depression, the percentage of patients
relapsing during continuation treatment with a 90mg weekly
dose was not significantly different from those taking a 20mg
daily dose. Weekly
dosing is recommended to begin seven days after the last daily
dose of 20mg.
Fluoxetine (under the trade name Sarafem) is now indicated for
the treatment of premenstrual dysphoric disorder
(PMDD). Because of
its long half-life, patients should allow at least five weeks
between discontinuation of fluoxetine and MAOI therapy.
Sertraline (Zoloft®): Sertraline is widely used in the treatment of depression. In addition to serotonergic activity, this drug causes some minor blockade of dopamine reuptake, which can lead to extrapyramidal side effects. It causes minimal anticholinergic, and sexual dysfunction. Sertraline has been associated with more cases of diarrhea than fluoxetine, but with fewer cases of anxiety and insomnia. At high doses, sertraline is an inhibitor of the CYP2D6 enzyme, but clinically significant drug interactions are unusual. The usual starting dose is 50 mg per day and dosage may be titrated to a range of 100 to 200 mg per day in a single or divided daily dose.
Paroxetine (Paxil®):
In the treatment of depression, paroxetine is initiated at a
dosage of 20 mg per
day. The upper
limit of the dosage range is 40 to 60 mg per
day. The side
effect profile of paroxetine is similar to that of the other
SSRIs, except that paroxetine tends to be more sedating and
anticholinergic.
It should probably be avoided in patients in whom the
anticholinergic activity would be undesirable, such as those
with Alzheimer’s disease or other cognitive
disorders. The
potential for weight gain, drug interactions, and sexual
dysfunction tends to be slightly higher with paroxetine than
with fluoxetine and sertraline.
Paroxetine has a
half-life of twenty hours and no metabolites; thus patients
are more prone to have withdrawal symptoms such as headache,
nausea, insomnia, and anxiety if doses are missed.
Recently, Paxil CR was brought to market in an attempt to
decrease the gastrointestinal side effects of
immediate-release
paroxetine. The
recommended initial dosage for the treatment of depression is
25mg per day, with a range of 25 to 62.5mg per
day. Patients
should be counseled that the tablets are to be swallowed whole
and not crushed or
chewed.
Citalopram (Celexa®): Citalopram has been associated with low rates of insomnia, anxiety, and other activating side effects. Nausea is the most common early side effect, but it should be transient. Citalopram has a relatively long half-life; thus it is less likely to cause a withdrawal syndrome compared with shorter acting SSRIs. The dose range of citalopram is 20 to 60 mg per day; the higher dose is typically used in the treatment of OCD. No clinically significant drug interactions have been documented. This drug may be appropriate in patients who take multiple medications because of its low potential for drug interactions.
Escitalopram (Lexapro®): Escitalopram oxalate is the S-enantiomer of citalopram. Escitalopram is the newest and most selective SSRI approved by the FDA for the treatment of depression, and is also useful in conditions for which other selective serotonin reuptake inhibitors have proven beneficial, such as anxiety disorders and PMDD. The most notable difference between escitalopram and citalopram is its potency. Clinical studies suggest that the efficacy of 10mg/day of escitalopram is comparable to 40mg/day of citalopram. An earlier onset of action of escitalopram relative to citalopram has also been suggested. The side effect profiles of the two agents are quite similar. As with citalopram, the potential for drug interactions is low.
Fluvoxamine (Luvox®): Fluvoxamine is FDA-approved only for the treatment of OCD in patients who are at least eight years of age. It is also used in the treatment of depression and anxiety disorders. The initial dosage in adults is 50mg daily, titrating up to 250 mg per day divided into two doses. Children can be started on a dosage of 25mg at bedtime, increasing every week to a maximum of 200mg per day in divided doses. The most common side effects are nausea, vomiting, and headache. Clinically important drug interactions with fluvoxamine are documented. These drug interactions are due to fluvoxamine’s potent inhibitory action at the cytochrome p-450 system.
Atypical Antidepressants
Venlafaxine
(Effexor®):
This agent is a potent serotonin and norepinephrine reuptake
inhibitor. Some
people now refer to this class as
SNRIs. Whether or
not the “dual action” of venlafaxine makes it more effective
than SSRIs is an area of
research. There
has been the suggestion in the literature that venlafaxine may
be more effective acutely for severely depressed patients
compared with
SSRIs. Again, this
will require further
study. The side
effect profile is comparable to that of the SSRIs and lower
than that of the tricyclic
antidepressants.
Anticholinergic side effects are significantly less severe
than those encountered with other
antidepressants.
Sexual side effects are similar to side effects caused by
SSRIs. Venlafaxine
can cause elevations in diastolic blood
pressure. However,
analyses show that this phenomenon is significant only with a
dosage above 300mg
daily.
Venlafaxine was first released in an immediate-release form
that is taken two or three times
daily. In 1997, an
extended-release form (Effexor XR) was approved by the FDA,
allowing for once-daily
administration.
The gastrointestinal side effects are less with the
extended-release
formulation. The
starting dose venlafaxine XR is 37.5 mg to 75 mg per
day. The dosage
may be titrated weekly to a maximum recommended dosage of
225mg per day.
Occasionally, patients with refractory depression will be
responsive to a dosage of 300mg daily.
Mirtazapine (Remeron®): Mirtazapine is unique in its action. Its primary effects appear to be antagonism of presynaptic a 2 autoreceptors and heteroreceptors that prevent release of norepinephrine and serotonin. The net result is an increase in both norepinephrine and serotonin in the synapse. In addition to this, the drug blocks 5-HT2A and 5-HT3 receptors. Blockade of these receptors leads to fewer activating side effects, less sexual dysfunction, and fewer gastrointestinal effects compared with other antidepressants. Mirtazapine has a high affinity for histamine receptors and can thus cause sedation and weight gain. There is a very small risk of neutropenia and agranulocytosis with mirtazapine. The recommended starting dosage is 15mg at bedtime, which may be titrated up to 45mg daily, if needed.
Trazodone (Desyrel®): This drug is a serotonin reuptake inhibitor that also blocks the 5-HT2A receptors. It has few anticholinergic side effects, but can cause orthostatic hypotension. Priapism can occur in men while taking trazodone. Because of its sedating effect, it is now frequently used in combination with other antidepressants for insomnia treatment.
Nefazodone (Serzone®): Nefazodone is a relative of trazodone with some pharmacological differences. It too is a 5-HT 2A antagonist, but also blocks the reuptake of serotonin and norepinephrine. Unlike trazodone, it causes minimal effects on sexual function, and is less likely to cause orthostatic hypotension. In January 2002, the FDA and the manufacturer of nefazodone added a black box warning concerning rare cases of liver failure. Nefazodone therapy should be avoided in patients with active liver disease or elevated serum transaminase levels, and discontinued when transaminase levels are three times the upper limit of normal or more. Patients taking nefazodone should be counseled on the signs and symptoms of liver failure, including jaundice, anorexia, gastrointestinal problems, and malaise. Nefazodone use is limited, most likely because of its numerous drug interactions. It is a potent inhibitor of CYP 3A4, which is the pathway responsible for most drugs metabolized in the liver.
Bupropion (Wellbutrin®): This drug is primarily an inhibitor of dopamine and norepinephrine reuptake and has minimal effects on serotonin. However, its exact mechanism of action remains to be defined. The drug has a short half-life and must be dosed TID unless the extended-release form is used, which is dosed BID. The sustained-release product may also cause fewer side effects and has largely replaced the immediate-release tablets. The most notable side effect of bupropion is increase seizure risk. This can be minimized by avoiding use in susceptible patients, such as those with epilepsy, and also not giving more than 150mg per dose or 450mg per day (400mg SR). Slow titration also decreases the risk of seizures. The most common side effects include nervousness, headache, and insomnia. Administering the second dose in the afternoon versus the nighttime can prevent insomnia. Given its potentiation of dopamine, bupropion can exacerbate psychosis. Bupropion may actually improve sexual function so it may be useful in treating depression in patients who suffer this side effect with other agents. Bupropion can also be added to an SSRI to treat sexual dysfunction. It is used for smoking cessation and marketed under the name of Zyban®.
Duloxetine (Cymbalta®): Duloxetine is a potent reuptake inhibitor of both serotonin and norepinephrine, which is similar to venlafaxine’s pharmacological activity. Duloxetine appears to have low affinity for other neurotransmitter systems. Duloxetine has been approved for the treatment of depression and will be comarketed under the trade name Cymbalta by Eli Lilly and Company. Duloxetine appears to be generally well tolerated. Common side effects in clinical trials were nausea, dry mouth, fatigue, somnolence, insomnia, and asthenia. It may also have minimal effects on sexual function, although effects have not been evaluated in a study designed specifically to assess adverse effects. Because duloxetine is pharmacologically related to venlafaxine, it will be important for providers to monitor for cardiovascular effects until large-scale data is available. Research does suggest that duloxetine may moderately inhibit the metabolism of drugs metabolized via CYP2D6 enzyme. Duloxetine has been administered as a 60mg single daily dose and also as a 40mg twice-daily dose. Duloxetine is also under investigation for the treatment of stress urinary incontinence in women. Serotonin and norepinephrine have been implicated in neural control of the lower urinary tract.
Treatment Resistance: Augmentation Therapy
Ten to 30 percent of patients taking antidepressants are
partially or totally resistant to the
treatment. Some
patients may also experience breakthrough or recurrence of
depression while taking the
medication.
Antidepressant combinations or augmentation may be
beneficial.
Combination therapy with multiple neurotransmitter activity
may be used, especially for treatment refractory
depression. Using
a second antidepressant may offset a side effect of another,
for example, using trazodone to treat SSRI induced insomnia or
using bupropion to treat sexual dysfunction associated with
SSRIs or venlafaxine.
Augmentation is a useful strategy in patients with a partial
response. The
best-documented options are lithium and
levothyroxine.
Lithium is administered in the usual dosages, keeping the
lithium blood levels to the lower end of the therapeutic range
(0.4 to 0.8 mEq per
L). Lithium may
increase serotonin
function. The
augmentation dosage of levothyroxine is 25mcg per
day. The effect is
not dependent upon thyroid
dysfunction. If
levothyroxine is used, cardiac status and thyroid hormone
levels must be
monitored.
Case reports and open studies indicate that augmentation with
the psychostimulant methylphenidate (Ritalin, in a dose of 5mg
to 40mg per day) can be
effective. Caution
should be taken when combining methylphenidate or other
psychostimulants with antidepressants that are
activating.
Antidepressant-Induced Sexual Dysfunction
Sexual
dysfunction, usually delayed ejaculation or anorgasmia, may
occur in both men and women who are taking SSRIs, venlafaxine,
and others. There
are several options in reducing this occurrence: decreasing
the dosage, switching to another agent, or adding another
agent to overcome the sexual side
effects. Sexual
dysfunction typically reverses within one to three days after
discontinuation of the antidepressant and returns on
reintroduction.
Due to its longer half-life, the recovery period may be one to
three weeks with
fluoxetine.
Uncontrolled studies and case reports suggest that the
addition of bupropion, cyproheptadine, nefazodone, or
mirtazapine may decrease sexual side
effects. In
patients with antidepressant-induced erectile dysfunction,
sildenafil (Viagra) may be useful if the patient has no
history of angina and is not taking nitrates.
Drug Interactions
The
choice of an appropriate antidepressant should include
consideration of drug-drug
interactions.
These interactions occur when SSRIs and other antidepressants
are coadministered with drugs metabolized via the cytochrome
P450 system. Two
of the isoenzymes of the cytochrome P450 system, 2D6 and 3A4,
are responsible for the metabolism of over 80% of currently
marketed drugs.
Table 3 summarizes the cytochrome P450 drug interactions
involving antidepressants.
Conclusion
Great
strides have been made over the last two decades in the
treatment of depression. Today we have antidepressants that
effectively treat depression with few side effects.
However, much remains to be understood as to how the
antidepressants work in
treatment.
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