Mood
Disorders and
Suicide
Mood disorders, also called affective disorders,
are pervasive alterations in emotions that are manifested
by depression, mania, or both. They interfere
with a person’s life, plaguing him or her with drastic
and long-term sadness, agitation, or elation. Accompanying
self-doubt, guilt, and anger alter life activities
especially those that involve self-esteem, occupation,
and relationships.
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• From early history, people have suffered from
• mood disturbances. Archaeologists have found holes
• drilled into ancient skulls to relieve the “evil humors”
• of those suffering from sad feelings and strange
behaviors.
• Babylonians and ancient Hebrews believed
• that overwhelming sadness and extreme behavior
• were sent to people through the will of God or other
• divine beings.
2
• Until the mid-1950s no treatment was available
• to help people with serious depression or mania. These
• people suffered through their altered moods, thinking
• they were hopelessly weak to succumb to these
devastating
• symptoms. Family and mental health professionals
• tended to agree, seeing sufferers as egocentric
• or viewing life negatively. While there are still no cures
• for mood disorders, effective treatments for both
depression
• and mania are now available.
3
CATEGORIES OF MOOD DISORDERS
• The primary mood disorders are major
depressive
• disorder and bipolar disorder (formerly called
manicdepressive
• illness). A major depressive episode lasts
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• at least 2 weeks, during which the person experiences
• a depressed mood or loss of pleasure in nearly all
• activities. In addition, four of the following symptoms
• are present: changes in appetite or weight, sleep,
• or psychomotor activity; decreased energy; feelings
• of worthlessness or guilt; difficulty thinking,
concentrating,
• or making decisions; or recurrent thoughts
• of death or suicidal ideation, plans, or attempts. These
• symptoms must be present every day for 2 weeks
• and result in significant distress or impair social,
• occupational, or other important areas of functioning
• (American Psychiatric Association [APA], 2000).
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• Some people also have delusions and hallucinations;
• the combination is referred to as psychotic depression.
• Bipolar disorder is diagnosed when a person’s
• mood cycles between extremes of mania and
depression
• (as described above). Mania is a distinct period
• during which mood is abnormally and persistently
• elevated, expansive, or irritable. The period lasts
• 1 week (unless the person is hospitalized and treated
• sooner).
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MANIA
• At least three of the following symptoms
• accompany the manic episode:
• inflated self-esteem
• or grandiosity; decreased need for sleep; pressured
• speech (unrelenting, rapid, often loud talking without
• pauses); flight of ideas (racing thoughts, often
• unconnected); distractibility; increased involvement
• in goal-directed activity or psychomotor agitation;
• and excessive involvement in pleasure-seeking activities
• with a high potential for painful consequences
• (APA, 2000).
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• Hypomania
• is a period of abnormally and persistently elevated,
• expansive, or irritable mood lasting 4 days and
including
• three or four of the additional symptoms described
• earlier. The difference is that hypomanic episodes do
• not impair the person’s ability to function (in fact he
• or she may be quite productive) and there are no
psychotic
• features (delusions and hallucinations).
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• Bipolar I disorder—one or more manic or
• mixed episodes usually accompanied by
• major depressive episodes
• • Bipolar II disorder—one or more major
• depressive episode accompanied by at least
• one hypomanic episode
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RELATED DISORDERS
• Other disorders classified in the DSM-IV-TR (2000)
• as mood disorders but with symptoms that are less
• severe or of shorter duration include the following:
• • Dysthymic disorder is characterized by at
• least 2 years of depressed mood for more
• days than not with some additional less severe
• symptoms that do not meet the criteria for a
• major depressive episode.
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• Cyclothymic disorder is characterized by
• 2 years of numerous periods of both hypomanic
• symptoms that do not meet the criteria
• for bipolar disorder.
• • Substance-induced mood disorder is
characterized
• by a prominent and persistent disturbance
• in mood that is judged to be a direct
• physiological consequence of ingested substances
• such as alcohol, other drugs, or toxins.
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• Mood disorder due to a general medical
condition
• is characterized by a prominent and
• persistent disturbance in mood that is judged
• to be a direct physiological consequence of a
• medical condition such as degenerative
• neurological conditions, cerebrovascular
• disease, metabolic or endocrine conditions,
• autoimmune disorders, HIV infections, or
• certain cancers.
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Other disorders that involve changes in mood
include the following:
• Seasonal affective disorder (SAD) has
• two subtypes. In one, most commonly called
• winter depression or fall-onset SAD, people
• experience increased sleep, appetite, and
• carbohydrate cravings; weight gain; interpersonal
• conflict; irritability; and heaviness
• in the extremities beginning in late autumn
• and abating in spring and summer.
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• Postpartum or “maternity” blues
• are a frequent normal experience after delivery
of ababy characterized by labile mood and affect,
• crying spells, sadness, insomnia, and anxiety.
• Symptoms begin approximately 1 day after
• delivery, usually peak in 3 to 7 days, and
• disappear rapidly with no medical treatment
• (Jones & Venis, 2001).
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• Postpartum depression meets all the criteria
• for a major depressive episode with onset
• within 4 weeks of delivery.
• • Postpartum psychosis is a psychotic episode
• developing within 3 weeks of delivery
beginning
• with fatigue, sadness, emotional lability,
• poor memory, and confusion and progressing
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• to delusions, hallucinations, poor insight and
• judgment, and loss of contact with reality.
• This medical emergency requires immediate
• treatment (Jones & Venis, 2001).
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ETIOLOGY
• Various theories for the etiology of mood disorders
• exist. Most recent research focuses on chemical biologic
• imbalances as the cause. Nevertheless psychosocial
• stressors and interpersonal events appear to
• trigger certain physiologic and chemical changes in
• the brain, which significantly alter the balance of
• neurotransmitters (Gabbard, 2000). Effective treatment
• addresses both the biologic and psychosocial
• components of mood disorders. Thus nurses need a
• basic knowledge of both perspectives when working
• with clients experiencing these disorders.
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Biologic Theories
• GENETIC THEORIES
• Genetic studies implicate the transmission of major
depression in first-degree relatives, who have twice the
risk of developing depression compared with the
• general population (APA, 2000). First-degree relatives
• of people with bipolar disorder have a 3% to 8% risk
• of developing bipolar disorder compared with a 1%
• risk in the general population.
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NEUROCHEMICAL THEORIES
• Neurochemical influences of neurotransmitters
(chemical
• messengers) focus on serotonin and norepinephrine
• as the two major biogenic amines implicated
• in mood disorders. Serotonin (5-HT) has many roles
• in behavior: mood, activity, aggressiveness and
irritability,
• cognition, pain, biorhythms, and neuroendocrine
• processes (that is, growth hormone, cortisol,
• and prolactin levels are abnormal in depression).
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• Deficits of serotonin, its precursor tryptophan, or a
• metabolite (5HIAA) of serotonin found in the blood
• or cerebrospinal fluid occur in people with depression.
• Positron emission tomography scans
• demonstrate reduced metabolism in the prefrontal
• cortex, which may promote depression (Tecott, 2000).
• Norepinephrine levels may be deficient in depression
• and increased in mania. This catecholamine
• energizes the body to mobilize during stress and
• inhibits kindling.
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• Dysregulation of acetylcholine and dopamine
• also are being studied in relation to mood
disorders.
• Cholinergic drugs alter mood, sleep,
neuroendocrine
• function, and the electroencephalographic
pattern;
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NEUROENDOCRINE INFLUENCES
• Hormonal fluctuations are being studied in relation
• to depression. Mood disturbances have been
documented
• in people with endocrine disorders such as
• those of the thyroid, adrenal, parathyroid, and
pituitary.
• Elevated glucocorticoid activity is associated
• with the stress response, and evidence of increased
• cortisol secretion is apparent in about 40% of clients
• with depression with the highest rates found among
• older clients.
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• Postpartum hormone alterations precipitate
• mood disorders such as postpartum depression
• and psychosis. About 5% to 10% of people with
• depression have thyroid dysfunction, notably an
elevated
• thyroid-stimulating hormone (TSH). This problem
• must be corrected with thyroid treatment or
treatment
• for the mood disorder will be affected adversely
• (Thase, 2000).
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Psychodynamic Theories
• Many psychodynamic theories about the cause of
mood disorders seemed to “blame the victim”
and his or her family (Gabbard, 2000):
• Freud looked at the self-depreciation of people
• with depression and attributed that self-reproach
• to anger turned inward related to
• either a real or perceived loss. Feeling
• abandoned by this loss, people became angry
• while both loving and hating the lost object.
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• Bibring believed that one’s ego (or self)
aspired
• to be ideal (that is, good and loving, superior
• or strong), and that to be loved and worthy,
• one must achieve these high standards.
• Depression results when, in reality, the person
• was not able to achieve these ideals all
• the time.
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• • Most psychoanalytical theories of mania
• view manic episodes as a “defense” against
• underlying depression, with the id taking
• over the ego and acting as an undisciplined,
• hedonistic being (child).
• • Meyer viewed depression as a reaction to a
• distressing life experience such as an event
• with psychic causality.
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CULTURAL CONSIDERATIONS
• Other behaviors considered age-appropriate can mask
• depression, which makes the disorder difficult to
• identify and diagnose in certain age groups. Children
• with depression often appear cranky. They may have
• school phobia, hyperactivity, learning disorders, failing
• grades, and antisocial behaviors. Adolescents
• with depression may abuse substances, join gangs,
• engage in risky behavior, be underachievers, or drop
• out of school. In adults, manifestations of depression
• can include substance abuse, eating disorders,
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• Many somatic ailments (physiologic ailments)
• accompany depression. This manifestation varies
• among cultures and is more apparent in cultures that
• avoid verbalizing emotions. For example, Asians
• who are anxious or depressed are more likely to have
• somatic complaints of headache, backache, or other
• symptoms. Latin cultures complain of “nerves” or
• headaches; Middle Eastern cultures complain of heart
• problems (Andrews & Boyle, 2003).
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MAJOR DEPRESSIVE DISORDER
• Major depressive disorder typically involves 2 or more
• weeks of a sad mood or lack of interest in life activities
• with at least four other symptoms of depression
• such as anhedonia and changes in weight, sleep,
• energy, concentration, decision-making, self-esteem,
• and goals. Major depression is twice as common in
• women and has a 1.5 to 3 times greater incidence in
• first-degree relatives than in the general population.
• Incidence of depression decreases with age in
• women and increases with age in men. Single and
• divorced people have the highest incidence. Depression
• in prepubertal boys and girls occurs at an equal
• rate (Kelso, 2000).
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Onset and Clinical Course
• An untreated episode of depression can last 6 to 24
• months before remitting. Fifty to sixty percent of
people
• who have one episode of depression will have another.
• After a second episode of depression, there is a
• 70% chance of recurrence. Depressive symptoms can
• vary from mild to severe. The degree of depression is
• comparable to the person’s sense of helplessness and
• hopelessness. Some people with severe depression
• (9%) have psychotic features (APA, 2000).
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Treatment and Prognosis
OF M.D
• PSYCHOPHARMACOLOGY
• Major categories of antidepressants include
cyclic antidepressants,
• monoamine oxidase inhibitors (MAOIs),
• selective serotonin reuptake inhibitors (SSRIs),
and atypical anti-depressants.
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• SSRIs. SSRIs, the newest category of antidepressants
• , are effective for most clients. Their
• action is specific to serotonin reuptake inhibition;
• these drugs produce few sedating, anticholinergic,
• and cardiovascular side effects, which makes them
• safer for use in children and older adults. Because of
• their low side effects and relative safety, people using
• SSRIs are more apt to be compliant with the treatment
• regimen than clients using more troublesome
• medications.
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• TCAs are contraindicated in severe impairment
• of liver function and in myocardial infarction (acute
• recovery phase). They cannot be given concurrently
• with MAOIs. Because of their anticholinergic side
• effects, TCAs must be used cautiously in clients who
• have glaucoma, benign prostatic hypertrophy, urinary
• retention or obstruction, diabetes mellitus,
hyperthyroidism,
• cardiovascular disease, renal impairment,
• or respiratory disorders
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• Fluoxetine (Prozac) produces a slightly higher
• rate of mild agitation and weight loss but less
somnolence. It has a half-life of more than 7 days,
which differs from the 25-hour half-life of other
SSRIs. Overdosage of TCAs occurs over several
days and
• results in confusion, agitation, hallucinations,
hyperpyrexia,
• and increased reflexes. Seizures, coma, and
• cardiovascular toxicity can occur with ensuing
tachy
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• Tetracyclic Antidepressants. Amoxapine
(Asendin) may cause extrapyramidal
symptoms, tardive dyskinesia, It can
• create tolerance in 1 to 3 months. It increases
appetite
• and causes weight gain and cravings for
sweets.
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• Atypical Antidepressants. Atypical
antidepressants
• are used when the client has an inadequate
response
• to or side effects from SSRIs. Atypical
antidepressants
• include venlafaxine (Effexor), bupropion
(Wellbutrin),
• nefazodone (Serzone), and mirtazapine
(Remeron).
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• Venlafaxine blocks the reuptake of serotonin,
• norepinephrine, and dopamine (weakly).
Bupropion
• modestly inhibits the reuptake of norepinephrine,
• weakly inhibits the reuptake of dopamine, and
has no
• effects on serotonin. Bupropion is marketed as
Zyban
• for smoking cessation.
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• MAOIs. This class of antidepressants is used
infrequently
• because of potentially fatal side effects and
• interactions with numerous drugs, both
prescription and over-the counter
preparations
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• life-threatening condition that can result when a
• client taking MAOIs ingests tyramine-containing
• foods and fluids or other medications. Symptoms
are
• occipital headache, hypertension, nausea,
vomiting,
• chills, sweating, restlessness, nuchal rigidity,
dilated
• pupils, fever, and motor agitation. These can lead
• to hyperpyrexia, cerebral hemorrhage, and death.
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OTHER MEDICAL TREATMENTS
AND PSYCHOTHERAPY
• Electroconvulsive Therapy. Psychiatrists may
use
• electroconvulsive therapy (ECT) to treat
depression
• in select groups such as clients who do not
respond
• to antidepressants or those who experience
• intolerable side effects at therapeutic doses
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• In addition, pregnant
• women can safely have ECT with no harm to
• the fetus. Clients who are actively suicidal may be
• given ECT if there is concern for their safety while
• waiting weeks for the full effects of
antidepressant
• medication.
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• ECT involves application of electrodes to the
• head of the client to deliver an electrical
impulse to
• the brain; this causes a seizure. It is believed
that the
• shock stimulates brain chemistry to correct
the chemical
• imbalance of depression.
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• Clients usually are given a series of 6 to 15 treatments
• scheduled 3 times a week. Generally a minimum
• of 6 treatments is needed to see sustained
• improvement in depressive symptoms. Maximum
• benefit is achieved in 12 to 15 treatments.
• Preparation of a client for ECT is similar to preparation
• for any outpatient minor surgical procedure.
• The client is NPO after midnight, removes any
• fingernail polish, and voids just prior to the procedure.
• An IV is started for the administration of
• medication.
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• Initially the client receives a short-acting
• anesthetic
• so he or she is not awake during the procedure.
• Next he or she receives a muscle relaxant, usually
• succinylcholine, that relaxes all muscles to reduce
• greatly the outward signs of the seizure (e.g., clonic,
• tonic muscle contractions). Electrodes are placed on
• the client’s head: one on either side (bilateral), or both
• on one side of the head (unilateral). The electrical
• stimulation is delivered, which causes seizure activity
• in the brain that is monitored by an electroencephalogram
• (EEG). The client receives oxygen and is assisted
• to breathe with an ambu bag.
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• gins to waken after a few minutes. Vital signs are
• monitored, and the client is assessed for the return of
• a gag reflex.
• Following ECT treatment, the client may be
• mildly confused or disoriented briefly. He or she is
• very tired and often has a headache. The symptoms
• are just like those of anyone who has had a grand mal
• seizure. In addition, the client will have some
shortterm
• memory impairment.
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• Following a treatment,
• the client may eat as soon as he or she is hungry and
• usually will sleep for a period. Headaches are treated
• symptomatically.
• Unilateral ECT results in less memory loss for
• the client, but more treatments may be needed to see
• sustained improvement. Bilateral ECT results in
• more rapid improvement but with increased shortterm
• memory loss.
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