Diagnosing and Treating
Mood Disorders: The Science
and Ethics
Chris Trimble, Leo Huizar, Fredah Kabbech,
Megan Sieveke, Brandon Butler
Mood Disorders
Depression
• Can refer to either:
– A mood: a pervasive
and sustained
emotional response
– A clinical syndrome:
a combination of
emotional, cognitive
and behavioral
symptoms
How To Distinguish
Depression From Normal
Sadness
• The mood change is pervasive across situations and
persistent over time
• The mood change may occur in the absence of any
precipitating events
• The depressed mood is accompanied by impaired
ability to function in usual social and occupational
roles
• The change in mood is accompanied by a cluster of
additional signs and symptoms
• The nature or quality of the mood change may be
different from that associated with normal sadness
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Four Types of Symptoms
Associated With Mood
Disorders
Emotional
Cognitive
Somatic
Behavioral
Emotional Symptoms
• Depressed or dysphoric mood is the
most common and obvious symptom of
depression
• People who are depressed describe
themselves as feeling utterly gloomy,
dejected and despondent
• Manic patients experience euphoric like
symptoms
Cognitive Symptoms
• Involve changes in the way
people think about themselves
and their surroundings
• Depressed people may have
trouble concentrating and are
easily distracted
• Preoccupation with guilt and
worthlessness
• Manic patients report sped up
thoughts and ideas
Somatic Symptoms
• Related to basic
physiological or bodily
functions
• Include fatigue, aches
and pains, and serious
changes in appetite or
sleeping patterns
Behavioral Symptoms
• Changes in the things that
people do and the rate at
which they do them
• Psychomotor retardation
often accompanies the
onset of depression
• Manic patients show
energetic, provocative and
flirtatious behavior
Diagnosing Mood Disorders
• Defined in terms of
episodes
– discrete periods of
time in which the
person’s behavior is
dominated by either
a depressed or
manic mood
Major Depressive Episode
• Five or more of the following symptoms
must have been present during the
same two week period and represent a
change from previous functioning
• At least one of the symptoms is either
– Depressed mood
– Loss of interest or pleasure
Major Depressive Episode
Symptoms
• Depressed mood most
of the day, nearly every
day
• Diminished pleasure in
all, or almost all
activities
• Significant weight loss
(without dieting) or
weight gain
• Insomnia or
hypersomnia nearly
every day
• Psychomotor agitation
or retardation
• Fatigue or loss of
energy
• Feelings of
worthlessness or guilt
• Diminished ability to
think or concentrate
• Recurrent thoughts of
death or suicidal
ideation
Manic Episode
• A distinct period of abnormally and
persistently elevated, or expansive
mood, lasting at least one week
• During the period of mood disturbance,
three of more of the following symptoms
have persisted and have been present
to a significant degree
Manic Episode Symptoms
• Inflated self esteem
or grandiosity
• Decreased need for
sleep
• More talkative than
usual
• Flight of ideas
• Distractibility (drawn to
unimportant stimuli)
• Increase in goal
directed activity
• Excessive involvement
in pleasurable activities
that have a high
potential for painful
consequences
Mood Disorders
• Two primary types:
– Unipolar mood disorder: the person
experiences only episodes of depression
– Bipolar mood disorder: the person
experiences episodes of mania as well as
depression
Types of Mood Disorders and
Frequency
Types of Mood Disorders
• Unipolar Mood
Disorders
– Major Depressive
Disorder
– Dysthymic Disorder
• Bipolar Mood Disorders
– Bipolar I Disorder
– Bipolar II Disorder
– Cyclothymic Disorder
• Subtypes
Major Depressive Disorder
• One or more major
depressive episodes
• No manic or
unequivocal hypomanic
episodes
• Lifetime prevalence of
15%
• Major Depressive
Disorder 15% suicide
mortality
• VA 1991 Study
– Major Depressive
Disorder mortality 38.7%
– 13% no psychiatric
monitoring
Major Depressive Disorder
• Course is variable
– Some having episodes years apart, clusters of
episodes, and some with frequent episodes
throughout life
– Only about 20% have chronic episodes
• After the first episode, 50%- 60% chance of a
second , and a 5%-10% chance of a manic
episode (i.e. developing bipolar I disorder)
• After second episode, 70% chance of a third
• After third episode, 90% chance of a fourth
• The greater number of previous episodes is
an important risk factor for recurrence
Major Depressive Disorder
• By definition, Major Depressive Disorder
cannot be due to:
– Physical illness, alcohol, medication, or street
drug use.
– Normal bereavement.
– Bipolar Disorder
– 7Mood-incongruent psychosis (e.g.,
Schizoaffective Disorder, Schizophrenia,
Delusional Disorder, or Psychotic Disorder Not
Otherwise Specified).
Major Depressive Disorder
Co-occurring Disorders
• Substance Abuse
• Anxiety
– 80 to 90% of individuals with Major Depressive
Disorder also have anxiety symptoms (e.g.,
anxiety, obsessive preoccupations, panic attacks,
phobias, and excessive health concerns).
• Cancer, COPD (Chronic Obstructive
Pulmonary Disease), Pain, eating disorders
• Causation:
– Meds: steroids
– Diseases: hypothyroidism
Dysthymic Disorder
• Depressed mood for at least two years
• Never without at least two of the
following symptoms for more than two
months
– Poor appetite or overeating, insomnia or
hypersomnia, low energy, low self esteem,
poor concentration, feelings of
hopelessness
Dysthymic Disorder
• No major depressive episode during the
first two years
• Lifetime risk of 3%
Bipolar I Disorder
• One or more manic episodes
• Lifetime risk of 1%
These positron emission tomography scans of the brain of a person with bipolar disorder show the
individual shifting from depression, top row, to mania, middle row, and back to depression, bottom row,
over the course of 10 days.
Bipolar II Disorder
• One or more major depressive episodes
• At least one hypomanic episode
– A hypomanic episode is a less severe version of
a manic episode.
• No manic episodes
Subtypes of Mood Disorders
• Melancholia: describes a particularly
severe type of depression
• Psychotic features: when hallucinations
or delusions were present during the
most recent episode
• Rapid cycling: the person experiences
at least 4 episodes within a 12 month
period
Subtypes of Mood Disorders
• Postpartum Onset:
when episodes begin
within 4 weeks after
childbirth
• Seasonal affective
disorder: when the
onset of episodes is
regularly associated
with changes in
seasons
Prevalence of Mood Disorders
• Depression accounts
for more than 10
percent of all disabilities
in the US
• Younger generations
are experiencing higher
rates of depression, and
those who become
depressed are doing so
at an earlier age
• Depression affects 1314 million people each
year
Prevalence of Mood Disorders
• Ratio of unipolar to bipolar is at least 5:1
• Lifetime prevalence of all mood
disorders is 8%, ranked third behind
substance abuse disorders and anxiety
disorders
Gender Differences
• Women are two or three times more
vulnerable to depression than men
– Sex hormones, stressful life events,
childhood adversity, etc
– May be more likely to seek treatment
– May be more likely to be labeled as
depressed
• No differences seen in bipolar disorders
Children Statistics
• Up to 2.5% of children
in the US suffer from
depression
• Up to 8.3% of
adolescents in the US
suffer from depression
• Girls entering puberty
are twice as likely to
experience depression
as boys
Types of Causes
• Environmental Factors
• Psychological Factors
• Biological Factors
Environmental Factors:
Stress
– Levels of stress may vary from person to
person.
– Depressive episodes can make a person
more vulnerable to further episodes, so
small amounts of stress can activate
depression
• “Learner Helplessness”- after experiencing
chronic or repeated stressful events, people
can learn to feel helpless
Environmental Factors:
Substance Abuse
– Depression that is a result of drug abuse,
medication, or toxin exposure
– Associated with use and withdrawl from: alcohol,
amphetamine, cocaine, hallucinogens, inhalants,
opioids, phencyclidine, sedaitves, hypnotics and
anxiolytics
– Exposure or habitual use of chemicals can alter
brain structure and function resulting in
depression
Environmental Factors:
Childhood Difficulties
– Depression can develop in children who have
experienced a traumatic event including but not
limited to:
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Death of family member or friend
Natural disaster
Divorce
Loss of parent’s job, home, etc...
– Many of these children are emotionally damaged
or lack emotional development and often have
difficulties adjusting
– Traumatic Event may affect the development of
the Limibic System
Depression In Disease
• Estimated 1/3 people with
chronic disease have
depression.
• Alzheimer’s
– Boston Study
• 14% had history of depression
• HIV
– 1/3 estimated to have
depression
Continued…
• The rate for depression occurring with medical
illness*:
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Heart attack: 40-65%
Coronary artery disease (without heart attack): 18-20%
Parkinson's disease: 40%
Multiple sclerosis: 40%
Stroke: 10-27%
Cancer: 25%
Diabetes: 25%
*Reviewed by the doctors at The Cleveland Clinic Department of Psychiatry and Psychology.
Psychological Factors
• Cognitive Vulnerability
– People responding differently to the same
negative experience involving loss, failure
and disappointment
https://www.depressionadvances.com/animation/brainAnimations.html
HYPOTHYROIDISM
COMMON SYMPTOMS
Delayed reflexes
Depressed mood
Weight changes
Cardiac failure
Apathy
Appetite problems
Cold intolerance
Weight gain
Sleep problems
Brittle hair
Fatigue
Dry skin
Impaired concentration
Thoughts of suicide
Delusions
Decreased appetite
DEPRESSION
Biological Factors
• Neurotransmitters and Neurons
– The signal enters the neuron through the dendrite
and proceeds through the cell body to the axon
where it is switched from a electric signal to a
chemical one
– Theses chemical signals are called
neurotransmitters
• Neurotransmitters can fit into many receptors, but
receptor sites can only receive specific transmitters
• Upon release the transmitter is broken down by mono
amine oxidase (MAO) or its taken back in by the neuron
that released it, called “reuptake”
Biological Factors
• Of the 30 or so known
neurotransmitters, depression effects
Serotonin, Norepinephrine, and
Dopamine
• Depression has been linked to both low
and elevated Norepinephrine
concentrations.
Biological Factors:
Serotonin
• The permissive hypothesis
of serotonin function
postulates that the deficit in
central serotonergic
neurotransmission permits
the expression of bipolar
disorder but is not sufficient
to cause it.
– According to this theory,
both the manic and the
depressive phases of
bipolar illness are
characterized by low central
serotonin function but differ
in high versus low
norepinephrine activity.
Biological Factors:
Norepinephrine
• The catecholamine
hypothesis of affective
disorders proposes that
some forms of depression
are associated with a
deficiency of catecholamine
activity (particularly
norepinephrine) at
functionally important
andrengeric receptor sites in
the brain, whereas mania is
associated with a relative
excess.
Biological Factors:
Dopamine
• Evidence is
substantial that
enhanced dopamine
activity may play a
primary role in
psychotic
depression.
Biological Factors: Hormones
– About one half of all depressed persons have a
high level of the hormone cortisol in their blood
– A person with a depressive mood disorder may
not have their hypothalamus regulating the cortisol
production in the adrenal gland correctly
– Normal cortisol levels peak at 8:00a.m. and
4:00p.m. for non depressed person, while a
person with depression may have the hormone
released at a constant level
Biological Factors: Genetics
• There is a 1.5 to 3% greater chance for a
person to develop a depressive disorder if a
parent or sibling has it as well
– 50% of those with bipolar disorder have a parent
with history of clinical depression
– 25% of children of a parent who is bipolar develop
a depressive disorder
– 50-75% of children of two parents with bipolar
disorder develop a depressive disorder
Biological Factors: Twin
Studies
• If one twin develops depression there is a
76% chance that the other twin will develop a
disorder as well
– When raised apart the percentage is 67%
– Because this number is not closer to 100%, there
is indication that other factors are also responsible
• Fraternal twins have a 19% chance of
developing a depressive disorder if the other
develops one
Bipolar Causes
Relation to Person
w/Bipolar
2nd degree relative
Risk of Developing
Bipolar
1%
Sibling
3-7%
Fraternal Twin
15-25%
One Parent
15-30%
Both Parents
50-75%
Identical Twin
70%
Causes of Depression
• Depression has been
linked to size/function in
the temporal and frontal
lobes and the cingulate
gyrus. However, it is
unclear as to whether
the depression causes
the abnormalities or the
depression is a result of
the abnormalities.
Treatment of Mood Disorders
Treatments:
• Unipolar Mood Disorders
– Cognitive Behavioral Therapy
– Antidepressant Medication
• Bipolar Mood Disorders
– Lithium
– Anticonvulsant Medication
– Psychotherapy
• Others
– Electroconvulsive Therapy
– Vagus Nerve Stimulation
– Transcranial Magnetic Stimulation
Cognitive Behavioral Therapy
• CBT combines both
cognitive therapy and
behavioral therapy
– Cognitive Therapy
teaches a person how
certain thinking patterns
are causing their
symptoms-by giving them
a distorted picture of
what's going on in their
life, and making them
feel anxious, depressed
or angry for no good
reason, or provoking
them into ill-chosen
actions.
Cognitive Behavioral Therapy
– Behavioral Therapy helps patients weaken
the connections between troublesome
situations and their habitual reactions to
them. It also teaches them how to calm
their mind and body, so they can feel
better, think more clearly, and make better
decisions
Cognitive Behavioral Therapy
• Identification of Skill Deficits:
– Help patient to identify deficits so that they can
learn better ways to manage life
• Evaluation of Life-Experiences
– Help patient develop realistic expectations about
life, and help distinguish between what the patient
needs and what they want
• Self-talk
– Help patient identify negative self-talk, teach them
how to combat these thoughts and to replace
them with positive thought
Cognitive Behavioral Therapy
• Automatic thoughts
– Help patient identify negative automatic thoughts
and ways to replace these thoughts with positive
ones
• Irrational ideas and Beliefs
– Teach patient how to identify their irrational
thoughts and how to differentiate between
irrational and rational thought
• Overgeneralizing and Catastrophizing
– Help patient identify and change negative
overgeneralizations
Cognitive Behavioral Therapy
• Cognitive Distortions
– Help patient determine what evaluations
are distortions by providing objective
feedback of their evaluations of the world
• Pessimistic Thinking
– Help patient develop more optimistic view
of world
Treatment:
Antidepressants
• Four types of drugs are used in the
treatment of depression and other
associated mood disorders:
– Tricyclic antidepressants
– Monoamine Oxidase Inhibitor
– Selective Serotonin Reuptake
Inhibitors
– Serotonin Norepinephrine
Reuptake Inhibitors
Tricyclic Antidepressants
• From 1960s until late 1980s, tricyclic
antidepressants represented the major
pharmaceutical treatment for
depression
• They still provide the surest
antidepressant response for moderately
to severe depression
Tricyclic Antidepressants
• TCAs work by increasing the
concentration of norepinephrine and
serotonin in certain regions of the CNS
• TCAs impede the reuptake of
norepindephrine and serotonin
• They are safe and effective for up to
80% of patients
Tricyclic Antidepressants
• There are two broad chemical classes:
– Tertiary Amines
• They have a greater effect in boosting
serotonin than norepinephrine.
– amitriptyline, imipramine, trimipramine and doxepin
– Secondary Amines
• Greater increase of norepinephrine levels
– nortriptyline, desipramine, and protriptyline
Monoamine Oxidase Inhibitors
• MAOIs treat depression by inhibiting the
effect of monoamine oxidase which causes
the concentrations of serotonin,
norepinephrine and dopamine to increase
• Most doctors will not prescribe MAOIs unless
a patient is not responding to other
antidepressants
Monoamine Oxidase Inhibitors
• Definitely Effective
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Atypical Depression
Major Depression
Dysthymia
Melancholia
Panic Disorder
Bulimia
Atypical facial pain
Anergic Depression
Treatment-resistant
depression
– Parkinson’s Disease
• Other Possible Uses
– Obsessivecomplusive Disorder
– Narcolepsy
– Headache
– Chronic pain
syndrome
– Generalized anxiety
disorder
Selective Serotonin Reuptake
Inhibitors
• SSRIs work by inhibiting the reuptake of
serotonin into the neuron that made it
• Includes fluoxetine and paroxetine
Serotonin Norepinephrine
Reuptake Inhibitors
• This class of drugs is most recent
addition to the family of antidepressants
and has a structure and chemical profile
that distinguishes them both tricyclic
antidepressants and SSRIs.
• Work by increasing levels of Serotonin
and Norepinephrine by inhibiting their
re-absorption back into the cell.
Venlafaxine
• Venlafaxine inhibits
serotonin and
norepinephrine
reuptake without
significant effects on
muscarinic, cholinergic,
histaminic, or alphaandrenergic receptors.
• Therefore, venlafaxine
activity is similar to
tricyclics and SSRIs but
has a less adverse
side-effect profile.
Bupropin
• Bupropin is the newest drug for treating
depression, although the exact
neurochemical mechanism is not known
– Does not inhibit monoamine oxidase or inihibit the
reuptake serotonin and norepinephrine
– Does inhibit the reuptake of dopamine to some
extent
• It is a stimulant type drug that is used in the
treatment of major depression.
Treatments:
Antidepressants
• 50-65% of people given an
antidepressant show much
improvement over 3 months, compared
to 25-30% of people given a placebo.
– Indicates that although drug is effective,
antidepressants, like most medicines, may
have some benefits due to placebo affect
Treatments:
Antidepressants
• Medication must be used every day or
at every time prescribed. If not taken
correctly treatment will not be effective
and may have adverse effects.
• Antidepressants will usually take 1-2
weeks work, however some may take
up to six weeks
Treatments:
Antidepressants
• On the basis of clinical research and
experience, the consensus is that most
people can be taken off their
antidepressants after six to eight
months of clinical response without
doing worse than patients continuing on
the drug
Bipolar Treatments
• Psychiatric Management
• Acute Treatment
• Maintenance Treatment
Psychiatric Management
At this time, there
is no cure for
bipolar disorder;
however, treatment
can decrease the
associated
morbidity and
mortality.
Bipolar Treatments:
Lithium
• Lithium is prescribed to people with
bipolar disorder to even out the “highs”
and “lows.”
• Because bipolar disorder requires long
term treatment, a patient may have to
take Lithium for many years, often in
combination with other antidepressants
Bipolar Treatments:
Lithium
• Lithium interferes with the synthesis and
reuptake of chemical messengers by which
nerves communicate with each other
(neurotransmitters). Lithium also affects the
concentrations of tryptophan and serotonin in
the brain.
• Lithium's effects usually begin within one
week of starting treatment, and the full effect
is seen by 2 to 3 weeks.
Bipolar Treatment:
Anticonvulsants
• Often prescribed to patients who do not
respond to lithium
• Include carbamazepine (Tegretol) or
valproic acid (Depakene)
• More than 50% respond positively to
these drugs
• Reduce the frequency and severity of
relapse
Treatments:
Electroconvulsive Therapy
– Patient is put to sleep and temporarily paralyzed,
so that their muscles do not contract and cause
injuries like fractures. An electric current is then
run through the brain to initiate a seizure.
– ECT is sometimes the most effective, rapid
method of treating severe major depressive
disorder (MDD).
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•
for patients with poor response to medications,
poor tolerance of usual antidepressants,
severe vegetative symptoms,
or psychotic features
Treatment:
Vagus Nerve Stimulation
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•
VNS stimulates the limbic
system, a group of related
structures that affect mood,
motivation, sleep, appetite,
alertness and other factors
commonly altered by
depression.
VNS is delivered to the left
cervical vagus nerve by the
NeuroCybernetic Prosthesis
(NCPâ) System which is
implanted just under the skin in
the left chest area.
– Delivers a pre-programmed,
intermittent electrical pulse to
cervical vagus nerve 24 hours a
day
Transcranial Magnetic
Stimulation
• TMS is a procedure in
which the electrical
activity in the brain is
influenced by a
magnetic pulse.
• This procedure can be
used to alter function of
certain areas of the
brain, especially those
involved in depression
Side Effects of Treatments
Side Effects:
Tricyclics
• Initially:
• they cause blurred
vision
• Constipation
• Light-headedness when
standing or sitting up
suddenly
• Dry mouth
• Difficulty urinating
• Feelings of confusion
• Cognitive Dysfunction
– A small percentage of
people will have other
side effects such as:
• sweating, a racing
heartbeat, low blood
pressure, allergic skin
reactions or sensitivity
to the sun.
– Side effects usually
disappear once
therapeutic effects if
medication take hold
Side Effects:
Tricyclics
• More serious side effects, although rare,
can be aggravation of narrow angle
glaucoma and seizures
• Some tricyclic side effects relate to the
fact that these medications have similar
effects on other neurotransmitters in the
CNS, notably histamine and
acetylcholine
Drug Interactions:
Tricyclics
• Drug
• MAOIs
• Norepinephrine
pressure
arrhyhmias
• Phenothiazines
• Barbiturates
metabolism
• Cimetidine
heterocyclics
• Haloperidol
• Methylphanidate
heterocyclics
Interaction
Stroke, hypertension
Large increase in blood
and incidence of
Psychosis, agitation
Increase heteocyclic
Blocks metabolism of
Can block metabolism of
heterocyclics
Blocks metabolisms of
Side Effects:
MAIOs
• The side effects of MAOIs are generally
more severe or frequent than for other
antidepressants
Side Effects:
MAIOs
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Drowsiness
Constipation
Nausea
Diarrhea
Stomach upset
Fatigue
Dry mouth
Dizziness
Low blood pressure
Lightheadedness, especially
when getting up from a lying
or sitting position
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Decreased urine output
Decreased sexual function
Sleep disturbances
Muscle twitching
Weight gain
Blurred vision
Headache
Increased appetite
Restlessness
Shakiness
Trembling
Weakness
Increased sweating
Drug Interactions:
MAOIs
• Because of the extensive inhibition of
monoamine oxidase by MAOIs
enzymes raises the potential for a
number of drug interactions.
– Many of these interaction occur with overthe-counter medications
Drug Interactions:
MAOIs
Drug
Interaction
Other MAOIS
Increase risk for side effect;
covulsions
Hypertension; convulsions
TCAs, Carbamazepine,
Cyclobenzaprine
SSRIs
Stimulants (dextromamphetamine);
Busirone
Meperidine
Dextromethorphan
Direct Sympathomimetics
Indirect Sympathomimetics
Oral Hypoglycemics (insulin)
Fenfluramine, L-Tryptophan
Serotonin Syndrome
Increased blood pressure
Potentially fatal interaction
Brief psychosis
Increased blood pressure
Hypertensive crisis possible
May worsen hypoglycemia
Serotonin Syndrome possible
Food Interactions:
MAOIs
• Food Restrictions
• MAOIs inhibit
– Avoid:
monoamine oxidase in
• Cheese, overripe aged
gut that is responsible
fruit, fava beans,
sausage, salami, sherry,
for the break down of
liquors, sauerkraut,
tyramine. A build up of
monosodium glutamate,
pickled fish, brewer’s
tyramine can lead to a
yeast, beef and chicken
sudden increase in
liver, fermented
products, red wine
blood pressure and a
– Used in moderation
chance of heart attack
• Coffee, chocolate,
or stroke.
colas, tea, soy sauce,
beer, other wines
Side Effects:
SSRIs
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loss of appetite, weight loss
increased appetite, weight gain
allergic reactions
dry mouth
irritability / anxiety
sleeplessness
drowsiness
headache
shaking
dizziness
fits / convulsions
disturbance of sexual function (but
this is also a feature of depression)
sweating
bruising
manic or hypomanic behaviour
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shaking
dizziness
fits / convulsions
disturbance of sexual function
(but this is also a feature of
depression)
sweating
bruising
manic or hypomanic behaviour
abnormal movements
low sodium level
suicidal ideas
abnormal movements
low sodium level
suicidal ideas
Drug Interactions:
SSRIs
• Although the potential for interaction
does exist, SSRIs are not associated
with many of the interactions are seen
with other antidepressants
– Paroxetine and fluvoxamine have been
associated with increased bleeding when
given with wafarin
– Does not effect Lithium levels
Suicide and SSRIs
• There is evidence that the use of
antidepressants, especially SSRIs, can cause
an increase in suicidal thoughts, however it
does not show an increase in cases.
– A severely depressed patient, or those with bipolar
syndrome in a “low” phase, usually only have the
energy to focus on their low. As the medication
begins to take affect they will have an increase in
energy and suicidal thoughts as they transition
from their “low” or depressed episode. It is this
time when the patient is still in a “depressed state
of mind,” that they are able to think more about
and idealize suicide because oh their higher
energy level.
Side Effects:
SNRIs
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Nausea and vomiting
Dizziness
Insomnia
Sleepiness
Abnormal dreams
Constipation
Sweating
Dry mouth
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Yawning
Tremor
Gas
Anxiety
Agitation
Abnormal vision
Headache
Sexual dysfunction
Side Effects: Bupropin
• 28% of patients will lose five pounds or more
• 0.04% of patients will experience seizures
– Common: Agitation, constipation, diarrhea,
dizziness, dry mouth, headache, increased
perspiration, insomnia, nausea, vomiting
– Rare: Acne, blurred vision, chest pains, chill,
coordination problems, confusion,
decrease in white blood cell count,
fainting, fever,hair color change
Withdrawls:
SNRIs
• Stopping treatment with SNRIs,
especially when done suddenly, can
cause withdrawal-like symptoms:
– nausea, vomiting, anxiety, diarrhea, agitation,
confusion, headaches, nightmares, coordination
changes, or skin-tingling or shock-like sensations
» Sometimes referred to as discontinuation
syndrome
Side Effects:
Electroconvulsive Therapy
• Anxiety or nervousness
• Gastrointestinal distress
(nausea and diarrhea)
• Headache
• Insomnia
• Rash
• Slight weight loss
• Sexual impotence in men
(about 10%)
• Lose of interest in sex for
both men and women;
inability to achieve
orgasm
The Chris Pittman Case
• In 2001, the 12 year
boy shot and killed
his grandparents
while being under
the influence of
Zoloft, a popular
antidepressant for
the previous couple
of days
The Chris Pittman Case
• Defense attorneys argued that Chris
suffered adverse reactions to the drug
including akathisia (a neurological
reaction characterized by extreme
internal restlessness, which has been
associated with suicide and violence),
emotional blunting, mania and
psychosis with testimonies by Chris’s
aunt and sister
The Chris Pittman Case
• Former FDA scientist Dr. Richard Kapit, who
had approved Zoloft for human clinical trials
even testified in Chris’s defense stating that
some antidepressants can alter the behavior
of people under 18, causing mania and even
suicide
• Chris was charged and
sentenced as an adult on
February 15, 2005, and is
now serving 30 years in
prison
Ethics
Ethics
• Ethical issue arises
over a depressed
patients ability to make
decisions concerning
treatment.
• An elderly patient that
has been diagnosed
with depression has
recently become
gravely ill, requiring
dialysis.
Ethics
• If you are not given an effective dosage
of antidepressant medication, suicide
rates increase. Is the hit-or-miss method
of treatment with medication ethical?
• Untreated Depression has a high risk of
suicide that accompanies the disorder
Ethics
• 54% of patients with bipolar disorder are
misdiagnosed as having depression
• Misdiagnoses and treatment of patients with
bipolar disorder as having a unipolar disorder
can magnify the patients symptoms
• Many antidepressants can cause a patient with bipolar
disorder to have exaggerated and prolonged “highs” and
“lows”
• Should we be quick to treat Depression with
medication when misdiagnosis can have
serious consequences.
References
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Downing-Orr, Kristina. Rethinking Depression - Why Current Treatments Fail. 1st ed. New
York: Plenum Press, 1998.
Higgins, Edmund S. "Is Depression a Neurochemical or Neurodegenerative?." Current
Psychiatry 3.9 (2004): 39-40.
Kline, Nathan S., M.D., Factors in Depression, Rockland State Hospital, Raven Press
Books, Inc., 1974
Lazarus, Jeremy A. "Ethics in Split Treatment." Psychiatric Annals 31.10 (2001): 611-614.
Oltmanns, Thomas F., Case studies in Abnormal Psychology, 3rd, John Wiley and Sons,
Inc., 1991
Oltmanns, Thomas F., and Robert E. Emery. Abnormal Psychology. 5th ed. Upper Saddle
River: Prentice Hall, 2004.
Schatzberg, Alan F., and Charles B. Nemeroff. Textbook of Psychopharmacology. 2nd ed.
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1993
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<http://www.webmd.com/content/article/45/1663_51215.htm>.
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