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Diagnosing and Treating

Mood Disorders: The Scienceand Ethics

Chris Trimble, Leo Huizar, Fredah Kabbech,

Megan Sieveke, Brandon Butler



Mood Disorders



Depression Can refer to either:

± A mood: a pervasive

and sustainedemotional response

± A clinical syndrome:

a combination of

emotional, cognitiveand behavioral

symptoms



How To Distinguish

Depression From NormalSadness The mood change is pervasive across situations and

persistent over time

The mood change may occur in the absence of anyprecipitating events

The depressed mood is accompanied by impairedability to function in usual social and occupationalroles

The change in mood is accompanied by a cluster of additional signs and symptoms

The nature or quality of the mood change may bedifferent from that associated with normal sadness



Four Types of Symptoms

Associated With MoodDisorders Emotional

Cognitive Somatic

Behavioral





Cognitive Symptoms Involve changes in the way

people think about themselves

and their surroundings Depressed people may have

trouble concentrating and areeasily distracted

Preoccupation with guilt andworthlessness

Manic patients report sped upthoughts 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 everyday

Diminished pleasure inall, or almost allactivities

Significant weight loss

(without dieting) or weight gain

Insomnia or hypersomnia nearlyevery day

Psychomotor agitationor retardation

Fatigue or loss of energy

Feelings of worthlessness or guilt

Diminished ability to

think or concentrate Recurrent thoughts of

death or suicidalideation



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 presentto 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 goaldirected 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 hypomanicepisodes

Lifetime prevalence of 15%

Major DepressiveDisorder 15% suicide

mortality VA 1991 Study

± Major DepressiveDisorder mortality 38.7%

± 13% no psychiatricmonitoring



Major Depressive Disorder Course is variable ± Some having episodes years apart, clusters of

episodes, and some with frequent episodesthroughout life

± Only about 20% have chronic episodes

After the first episode, 50%- 60% chance of asecond , and a 5%-10% chance of a manicepisode (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 streetdrug 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 DepressiveDisorder also have anxiety symptoms (e.g.,anxiety, obsessive preoccupations, panic attacks,phobias, and excessive health concerns).

Cancer, COPD (Chronic ObstructivePulmonary 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 hallucinationsor delusions were present during themost recent episode

Rapid cycling: the person experiencesat least 4 episodes within a 12 monthperiod



Subtypes of Mood Disorders Postpartum Onset:

when episodes begin

within 4 weeks after

childbirth

Seasonal affective

disorder: when the

onset of episodes is

regularly associatedwith changes in

seasons



Prevalence of Mood Disorders Depression accounts

for more than 10percent of all disabilities

in the US Younger generations

are experiencing higher rates of depression, andthose who become

depressed are doing soat an earlier age

Depression affects 13-14 million people eachyear



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 asdepressed

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 toexperience 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 personmore vulnerable to further episodes, so

small amounts of stress can activate

depression

³Learner Helplessness´- after experiencing

chronic or repeated stressful events, people

can learn to feel helpless




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




Childhood Difficulties

± Depression can develop in children who haveexperienced a traumatic event including but not

limited to: Death of family member or friend

Natural disaster

Divorce

Loss of parent¶s job, home, etc...

± Many of these children are emotionally damagedor lack emotional development and often havedifficulties 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



C

ontinued« The rate for depression occurring with medical illness*:

± Heart attack: 40-65%

± C

oronary 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, failureand disappointment



https://www.depressionadvances.com/animation/brainAnimations.htmlhttps://www.depressionadvances.com/animation/brainAnimations.html



HYPOTHYROIDISM COMMON SYMPTOMS DEPRESSION

Delayed reflexes Depressed mood Weight changes

Cardiac failure Apathy A ppetite problems

Cold intolerance Weight gain Sleep problems

Brittle hair Fatigue

Dry skin Impaired concentration

Thoughts of suicide

Delusions

Decreased appetite



Biological Factors Neurotransmitters and Neurons

± The signal enters the neuron through the dendriteand proceeds through the cell body to the axonwhere it is switched from a electric signal to achemical one

± Theses chemical signals are calledneurotransmitters

Neurotransmitters can fit into many receptors, butreceptor sites can only receive specific transmitters

Upon release the transmitter is broken down by monoamine oxidase (MAO) or its taken back in by the neuronthat released it, called ³reuptake´



Biological Factors Of the 30 or so known

neurotransmitters, depression effects

Serotonin, Norepinephrine, andDopamine

Depression has been linked to both low

and elevated Norepinephrineconcentrations.



Biological Factors:

Serotonin The permissive hypothesis

of serotonin functionpostulates that the deficit incentral serotonergic

neurotransmission permitsthe expression of bipolar disorder but is not sufficientto cause it.

± According to this theory,both the manic and the

depressive phases of bipolar illness arecharacterized by low centralserotonin function but differ in high versus lownorepinephrine activity.



Biological Factors:

Norepinephrine The catecholamine

hypothesis of affectivedisorders proposes thatsome forms of depression

are associated with adeficiency of catecholamineactivity (particularlynorepinephrine) atfunctionally importantandrengeric receptor sites inthe brain, whereas mania is

associated with a relativeexcess.



Biological Factors:

Dopamine Evidence is

substantial that

enhanced dopamineactivity 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 maynot 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 hormonereleased 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 aparent 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



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%, thereis 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

Risk of Developing

Bipolar

2nd degree relative 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 thedepression is a result of

the abnormalities.







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 bothcognitive therapy andbehavioral therapy

± Cognitive Therapyteaches a person howcertain thinking patternsare causing their symptoms-by giving thema distorted picture of

what's going on in their life, and making themfeel anxious, depressedor angry for no goodreason, or provokingthem into ill-chosen

actions.




± Behavioral Therapy helps patients weaken

the connections between troublesome

situations and their habitual reactions tothem. It also teaches them how to calm

their mind and body, so they can feel

better, think more clearly, and make better

decisions




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 patientneeds and what they want

Self-talk ± Help patient identify negative self-talk, teach them

how to combat these thoughts and to replacethem with positive thought




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 negativeovergeneralizations




Cognitive Distortions

± Help patient determine what evaluations

are distortions by providing objectivefeedback of their evaluations of the world

Pessimistic Thinking

± Help patient develop more optimistic viewof 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 moderatelyto severe depression




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 to80% of patients




There are two broad chemical classes:

± Tertiary Amines

They have a greater effect in boostingserotonin 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 theeffect of monoamine oxidase which causesthe concentrations of serotonin,norepinephrine and dopamine to increase

Most doctors will not prescribe MAOIs unlessa patient is not responding to other antidepressants



Monoamine Oxidase Inhibitors

Definitely Effective ± Atypical Depression

± Major Depression

± Dysthymia ± Melancholia

± Panic Disorder

± Bulimia

± Atypical facial pain

± Anergic Depression ± Treatment-resistant

depression

± Parkinson¶s Disease

Other Possible Uses

± Obsessive-

complusive 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 profilethat distinguishes them both tricyclic

antidepressants and SSRIs.

Work by increasing levels of Serotoninand Norepinephrine by inhibiting their

re-absorption back into the cell.



Venlafaxine

Venlafaxine inhibitsserotonin andnorepinephrine

reuptake withoutsignificant effects onmuscarinic, cholinergic,histaminic, or alpha-andrenergic receptors.

Therefore, venlafaxineactivity is similar totricyclics and SSRIs buthas a less adverseside-effect profile.





Treatments:

Antidepressants 50-65% of people given an

antidepressant show much

improvement over 3 months, comparedto 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 effectiveand may have adverse effects.

Antidepressants will usually take 1-2

weeks work, however some may takeup 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 onthe 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 ³highs´

and ³lows.´ Because bipolar disorder requires long

term treatment, a patient may have to

take Lithium for many years, often incombination 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 oneweek 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 tothese 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 causeinjuries 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 depressivedisorder (MDD).

for patients with poor response to medications,

poor tolerance of usual antidepressants, severe vegetative symptoms,

or psychotic features



Treatment:

Vagus Nerve Stimulation VNS stimulates the limbic

system, a group of relatedstructures that affect mood,motivation, sleep, appetite,alertness and other factors

commonly altered bydepression.

VNS is delivered to the leftcervical vagus nerve by theNeuroCybernetic Prosthesis(NCPâ) System which isimplanted just under the skin inthe left chest area. ± Delivers a pre-programmed,

intermittent electrical pulse tocervical vagus nerve 24 hours aday



Transcranial Magnetic

Stimulation TMS is a procedure in

which the electrical

activity in the brain is

influenced by amagnetic pulse.

This procedure can be

used to alter function of

certain areas of thebrain, especially those

involved in depression



Side Effects of Treatments



Side Effects:

Tricyclics Initially:

they cause blurredvision

Constipation Light-headedness when

standing or sitting upsuddenly

Dry mouth

Difficulty urinating

Feelings of confusion

Cognitive Dysfunction

± A small percentage of

people will have other

side effects such as:

sweating, a racingheartbeat, low blood

pressure, allergic skin

reactions or sensitivity

to the sun.

± Side effects usually

disappear oncetherapeutic 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 theCNS, notably histamine and

acetylcholine



Drug Interactions:

Tricyclics Drug Interaction MAOIs Stroke, hypertension

Norepinephrine Large increase in blood

pressure and incidence of arrhyhmias

Phenothiazines Psychosis, agitation

Barbiturates Increase heteocyclicmetabolism

Cimetidine Blocks metabolism of heterocyclics

Haloperidol Can block metabolism of heterocyclics

Methylphanidate Blocks metabolisms of heterocyclics





Side Effects:

MAIOs Drowsiness

Constipation

Nausea

Diarrhea Stomach upset

Fatigue

Dry mouth

Dizziness

Low blood pressure Lightheadedness, especiallywhen getting up from a lyingor sitting position

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 anumber of drug interactions.

± Many of these interaction occur with over-

the-counter medications



Drug Interactions:

MAOIsDrug InteractionOther MAOIS Increase risk for side effect;

covulsions

TCAs, Carbamazepine, Hypertension; convulsions

Cyclobenzaprine

SSRIs Serotonin Syndrome

Stimulants (dextromamphetamine); Increased blood pressure

Busirone

Meperidine Potentially fatal interaction

Dextromethorphan Brief psychosisDirect Sympathomimetics Increased blood pressure

Indirect Sympathomimetics Hypertensive crisis possible

Oral Hypoglycemics (insulin) May worsen hypoglycemia

Fenfluramine, L-Tryptophan Serotonin Syndrome possible



Food Interactions:

MAOIs MAOIs inhibit

monoamine oxidase in

gut that is responsible

for the break down of tyramine. A build up of

tyramine can lead to a

sudden increase in

blood pressure and a

chance of heart attack

or stroke.

Food Restrictions ± Avoid:

Cheese, overripe agedfruit, fava beans,

sausage, salami, sherry,liquors, sauerkraut,monosodium glutamate,pickled fish, brewer¶syeast, beef and chickenliver, fermentedproducts, red wine

± Used in moderation

Coffee, chocolate,colas, tea, soy sauce,beer, other wines



Side Effects:

SSRIs 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

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 associatedwith 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 causean increase in suicidal thoughts, however it

does not show an increase in cases. ± A severely depressed patient, or those with bipolar syndrome in a ³low´ phase, usually only have theenergy to focus on their low. As the medicationbegins to take affect they will have an increase in

energy and suicidal thoughts as they transitionfrom their ³low´ or depressed episode. It is thistime when the patient is still in a ³depressed stateof mind,´ that they are able to think more aboutand idealize suicide because oh their higher

energy level.



Side Effects:

SNRIs Nausea and vomiting

Dizziness

Insomnia

Sleepiness

Abnormal dreams

Constipation

Sweating Dry mouth

Yawning

Tremor

Gas Anxiety

Agitation

Abnormal vision Headache

Sexual dysfunction

Side Effects: Bupropin



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:



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 grandparentswhile being under

the influence of

Zoloft, a popular

antidepressant for the previous couple

of days



The Chris Pittman Case

Defense attorneys argued that Chrissuffered adverse reactions to the drug

including akathisia (a neurologicalreaction characterized by extremeinternal restlessness, which has beenassociated with suicide and violence),

emotional blunting, mania andpsychosis with testimonies by Chris¶saunt and sister





Ethics



Ethics

Ethical issue arisesover a depressedpatients ability to make

decisions concerningtreatment.

An elderly patient thathas been diagnosedwith depression has

recently becomegravely ill, requiringdialysis.



Ethics

If you are not given an effective dosage

of antidepressant medication, suicide

rates increase. Is the hit-or-miss methodof treatment with medication ethical?

Untreated Depression has a high risk of suicide that accompanies the disorder



Ethics

54% of patients with bipolar disorder aremisdiagnosed as having depression

Misdiagnoses and treatment of patients withbipolar 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 ³highs´ and³lows´

Should we be quick to treat Depression withmedication when misdiagnosis can haveserious consequences.

References



References

Downing-Orr, K ristina. 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.

K line, Nathan S., M.D., Factors in Depression, Rockland State Hospital, Raven Press Books, Inc., 1974

Lazarus, Jeremy A. "Ethics in S plit Treatment." Psychiatric Annals 31.10 (2001): 611-614.

Oltmanns, Thomas F., Case studies in A bnormal Psychology, 3rd, John Wiley and Sons,

Inc., 1991 Oltmanns, Thomas F., and Robert E. Emery. A bnormal Psychology. 5th ed. U pper Saddle

River: Prentice Hall, 2004.

Schatzberg, Alan F., and Charles B. Nemeroff. Textbook of Psychopharmacology. 2nd ed. Washington: American Psychiatric Press Inc., 1998.

S pitzer, Robert L., Psychopathology, A case book, Columbia University, McGraw-Hill, Inc., 1993

Diagnostic and Statistical Manual of Mental Disorders. IV txt revision ed. Washington: American Psychiatric Association, 2000.

"Depression Caused by Chronic Illness."Web MD. July 2005. WebMD Inc.. 02 A pr. 2006 <http://www.webmd.com/content/article/45/1663_51215.htm>.

"Neurotransmitter Animation." Depression Advances. 2006. Eli Lilly and Company. 05 A pr. 2006 <https://www.depressionadvances.com/animation/brainAnimations.html>.



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Diag Treat Mood