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Module 5 Mood Disorders

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Module 5 Mood Disorders

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gowrisra5
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Module 5

Mood Disorders
• Mood Disorders:
• Types- Unipolar depressive disorders and Bipolar disorders
• Prevalence.
• Unipolar depressive disorders-
• Major depressive disorder- Different specifiers,
• Persistent depressive disorder (Dysthymic disorder),
• Premenstrual Dysphoric Disorder.
• Causal factors: Biological, Psycho social and Socio cultural factors.
• Treatment and outcome.
• Bipolar and related disorders-
• Cyclothymic disorder,
• Bipolar I disorder,
• Bipolar II disorder,
• Causal factors: Biological, Psychological factors.
• Treatment and outcome
Mood Disorders
• Formerly called affective disorders
• Extreme variations in mood—either low or high—as the
predominant feature.
• Becomes seriously maladaptive, even to the extent of suicide
• Mood disorders are serious changes in one’s mood that may lead
to distress and dysfunction.
• The two key moods involved in mood disorders are
• Mania – intense and unrealistic feelings of excitement and euphoria, and
• Depression – feelings of extraordinary sadness and dejection.
• Manic and depressive mood states are often conceived to be at opposite ends of a
mood continuum, with normal mood in the middle.
• Some people with mood disorders experience only time periods or episodes
characterized by depressed moods. (Unipolar)
• However, other people experience manic episodes at certain time and
depressive episodes at other times. (Bipolar)
• Normal mood states can occur between both types of episodes.
• In these mixed-episode cases, the person experiences rapidly alternating moods
such as sadness, euphoria, and irritability, all within the same episode of illness.
• i.e., mania and depression during the same time period.
Types of mood disorders
• Unipolar depressive disorders – person experiences only
depressive episodes,
• Bipolar and related disorders – person experiences both manic
and depressive episodes.
• Most common form of mood disturbance involves depression.
• To be diagnosed with major depressive disorder, a person must be
markedly depressed or lose interest in formerly pleasurable
activities (or both) for at least 2 weeks.
• Other symptoms are changes in sleep or appetite, or feelings of worthlessness
• Manic episode – person shows a markedly elevated, euphoric, or expansive mood
• often interrupted by occasional outbursts of intense irritability or even violence—particularly
when others refuse to go along with the manic person’s wishes and schemes.
• must persist for at least a week.
• three or more additional symptoms must occur in the same time period, ranging from
• behavioral symptoms (such as a notable increase in goal-directed activity,
• to mental symptoms where self-esteem becomes grossly inflated and mental activity may speed up
(such as a “flight of ideas” or “racing thoughts”),
• to physical symptoms (such as a decreased need for sleep or psychomotor agitation).
• Hypomanic episode – milder form of manic episode, similar kinds of symptoms
• person experiences abnormally elevated, expansive, or irritable mood for at least 4 days.
• at least three other symptoms similar to those involved in mania but to a lesser degree (e.g.,
inflated self-esteem, decreased need for sleep, flights of ideas, pressured speech, etc.).
• less impairment in social and occupational functioning in hypomania
• hospitalization is not required.
Prevalence of mood disorders
• Major mood disorders occur with alarming
frequency—at least 15 to 20 times more frequently
than schizophrenia, for ex, and at almost the same
rate as all the anxiety disorders taken together.
• Lifetime prevalence rates of unipolar major
depression are nearly 17%.
• Women are overly represented in unipolar
depression 2:1. This is found cross-culturally.
Postpartum
Blues
Postpartum “Blues”
• More common than postpartum depression
• Even though the birth of a child would usually seem to be a happy event,
postpartum depression sometimes occurs in new mothers (and occasionally
fathers) and it is known to have adverse effects on child outcomes
• The symptoms of postpartum blues typically include changeable mood, crying
easily, sadness, and irritability, often liberally intermixed with happy feelings
• 50%–70% of women experience the “blues” within 10 days of giving birth and
usually subside on their own
• Hypomanic symptoms are also frequently observed, intermixed with the more
depression-like symptoms
• A greater likelihood of developing major depression after the postpartum blues
Causes

• Hormonal readjustments and alterations in serotonin and


noradrenalin
• if the new mother has lack of social support
• has difficulty in adjusting to her new identity and
responsibilities,
• if the woman has a personal or family history of
depression that leads to heightened sensitivity to the
stress of childbirth
Premenstru
al Dysphoric
Disorder
Premenstrual Dysphoric Disorder
• This disorder is diagnosed if a woman has had a certain set of symptoms in the
majority of her menstrual cycles (in the final week before the onset of menses) for the
past year.
• Symptoms start to improve within a few days after the onset of menses, and become
minimal or absent in the week post-menses.
• This is one form of depression where hormones clearly play an important role.
At least one of the four symptoms must • There are seven other symptoms that are listed
and a total of five symptoms must be
occur :
experienced:
(1) marked affective lability such as mood (1) decrease interest in usual activities,
swings,
(2) subjective sense of difficulties in concentration;
(2) marked irritability or anger or increased (3) lethargy, easy fatigability, or lack of energy,
interpersonal conflicts
(4) marked changes in appetite or overeating,
(3) marked depressed mood, or feelings of (5) hypersomnia or insomnia,
hopelessness or self-deprecating thoughts, or
(6) a sense of being overwhelmed or out of control,
(4) marked anxiety, tension or feelings of and
being “keyed up” or “on edge.” (7) physical symptoms such as breast tenderness or
swelling, a sense of bloating, weight gain, etc.
Unipolar Depressive
Disorders
• Person experiences extraordinary sadness/ depression.
• On the basis of duration and severity of depressive symptoms,
unipolar mood disorder is classified into two types namely,
• Major Depressive Disorder (MDD) – More severe, shorter duration (at
least 2 weeks)
• Dysthymia/Persistent Mood Disorder – Less severe, longer duration (at
least 2 years)
• Generally, the symptoms of depression can be classified as
affective, cognitive, and physical.
Persistent Depressive
Disorder
• Earlier called Dysthymia
• Shares many features with Major Depressive Disorder, but is different in two regards.
• First, dysthymia has fewer and less intense symptoms (mild-to-moderate intensity) and
• Second, depression lasts for a long period.
• Chronic feeling of depression for at least 2 years.
• On an average, mild-moderate symptoms for 4-5 years, but in some cases, it may last for
20 years or more.
• In addition, individuals must have at least 2 of 6 additional symptoms when depressed.
1) Poor appetite or overeating.
2) Insomnia or hypersomnia.
3) Low energy or fatigue.
4) Low self-esteem.
5) Poor concentration or difficulty making decisions.
6) Feelings of hopelessness.
• Periods of normal mood may occur briefly, but they usually last
for only a few days to a few weeks (and for a maximum of 2
months).
• Intermittent normal moods also distinguishes dysthymic
disorder from MDD.
• Poorer outcomes and as much impairment as those with major
depression (because of its chronicity)
• Is common, with 2.5%–6% lifetime prevalence rates.
• Begins in adolescence, 50% of those seeking treatment have an
onset before the age of 21 and 74% recover within 10 years.
• Half relapse usually occurs at 71% after the 3-year follow up.
DSM-5 Criteria for Dysthymia/Persistent Depressive
Disorder
A. Depressed mood for most of the day, for more days than not, as indicated by either subjective account
or observation by others, for at least 2 years.
B. Presence, while depressed, of two (or more) of the following:
1) Poor appetite or overeating. 2) Insomnia or hypersomnia. 3) Low energy or fatigue. 4) Low self-esteem. 5) Poor
concentration or difficulty making decisions. 6) Feelings of hopelessness.

C. During the 2-year period (1 year for children or adolescents) of the disturbance, the individual has
never been without the symptoms in Criteria A and B for more than 2 months at a time. Criteria for a
major depressive disorder may be continuously present for 2 years.
D. There has never been a manic episode or a hypomanic episode, and criteria have never been met for
cyclothymic disorder.
E. The disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia,
delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder.
F. The symptoms are not attributable to the physiological effects of a substance (for example, a drug of
abuse, a medication) or another medical condition (for example, hypothyroidism).
G. The symptoms cause clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
Major Depressive Disorder
• More severe and persistant symptoms than are required for
dysthymia
• not interwoven with periods of normal mood
• Rule out mania, hypomania, or mixed episode.
• Markedly depressed moods or marked loss of interest in
pleasurable activities most of every day, nearly every day, for
at least 2 consecutive weeks.
• In addition to showing one or both of these symptoms, the person
must experience additional symptoms during the same period:
Five (or more) of the following symptoms present during the same 2-week period and
represent a change from previous functioning:
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels
sad, empty, or hopeless) or observation made by others (e.g., appears tearful). ( note: In children and
adolescents, can be irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every
day (as indicated by either subjective account or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body
weight in a month), or decrease or increase in appetite nearly every day. ( note: In children, consider
failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective
feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every
day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective
account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific
plan, or a suicide attempt or a specific plan for committing suicide.
DSM-5 Criteria for Major Depressive Disorder
A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous
functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, or hopeless) or observation made
by others (e.g., appears tearful). ( note: In children and adolescents, can be irritable mood.)
2. markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account
or observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in
appetite nearly every day. ( note: In children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about
being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for
committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or another medical condition.
D. The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic
disorders.
E. There has never been a manic episode or a hypomanic episode.
Recurrent Vs Relapse
• Depression is a recurrent disorder
• When a diagnosis of MDD is made, it is usually also specified whether this is a first, and therefore single
(initial), episode or a recurrent episode (preceded by one or more previous episodes).
• Depressive episodes are usually time limited; the average duration of an untreated episode is about 6 to
9 months.
• In approximately 10 to 20% MDD, the symptoms do not remit for over 2 years, in which case PDD is
diagnosed.
• Although most depressive episodes remit (which is not said to occur until symptoms have largely been gone
for at least 2 months), depressive episodes often recur at some future point.
• Between episodes a person suffering from MDD is essentially symptom free.
• Relapse refers to the return of symptoms within a fairly short period of time, a situation that probably
reflects the fact that the underlying episode of depression has not yet run its course.
• For ex, relapse may commonly occur when pharmacotherapy is terminated prematurely—after symptoms
have remitted but before the underlying episode is really over.
• 40-50 % will exhibit a recurrence (i.e., a new episode of depression) of MDD, although the time period
before a recurrence occurs is highly variable.
• Probability of recurrence increases with the number of prior episodes and also when the person has
comorbid disorders.
Specifiers for Major
Depressive Episodes
• Some individuals who have major depressive episode also
have additional patterns of symptoms or features that are
important to note when making a diagnosis
• because these patterns have implications for understanding
more about the course of the disorder and its most effective
treatment.
• These different patterns of symptoms or features are called
specifiers in DSM-5
Major depressive episode
with melancholic features
In addition to meeting the criteria for a major depressive
episode, a patient
• Either has lost interest or pleasure in almost all
activities or
• Does not react to usually pleasurable stimuli or desired
events.
• Show greater cognitive impairment
• More heritable than most other forms of depression
• Associated with a history of childhood trauma .
with Psychotic features
• Psychotic symptoms, characterized by loss of contact with reality and delusions (false
beliefs) or hallucinations (false sensory perceptions),
• Delusions or hallucinations are usually mood congruent—that is, they seem in some sense
appropriate to serious depression because the content is negative in tone, such as
themes of personal inadequacy, guilt, deserved punishment, death, or disease.
• For ex, the delusional idea that one’s internal organs have totally deteriorated—ties in with
the mood of a person who is despondent.
• Feelings of guilt and worthlessness
• Likely to have longer episodes, more cognitive impairment, and a poorer long-term
prognosis
• Any recurrent episodes are also likely to be characterized by psychotic symptoms.
• Treatment - antipsychotic medication as well as antidepressant
with Atypical features
• Mood reactivity; that is, the person’s mood brightens in response to potential positive
events.
• In addition, the person must show two or more of the four symptoms
• weight gain or increase in appetite,
• hypersomnia,
• leaden paralysis (arms and legs feel as heavy as lead),
• being acutely sensitive to interpersonal rejection.
• Disproportionate number of females
• Earlier-than-average age of onset
• More likely to show suicidal thoughts.
• Linked to a mild form of bipolar disorder that is associated with hypomanic (Bipolar II).
• Respond to a different class of antidepressants—the monoamine oxidase inhibitors
with Catatonic features

• Individual shows marked psychomotor disturbances.


• Includes a range of psychomotor symptoms, from motoric
immobility (catalepsy—a stuporous state) to extensive
psychomotor activity, as well as mutism and rigidity.

• Catatonia is known more as a subtype of schizophrenia,


but it is actually more frequently associated with certain
forms of depression and mania than with schizophrenia.
With Seasonal pattern
• Recurrent major depressive episode with a seasonal pattern,
• Also commonly known as seasonal affective disorder.
• At least two episodes of depression in the past 2 years occurring at the
same time of the year (most commonly fall or winter), and
• full remission must also have occurred at the same time of the year (most
commonly spring).
• In addition, the person cannot have had other, nonseasonal depressive
episodes in the same 2-year period, and most of the person’s lifetime
depressive episodes must have been of the seasonal variety.
• More common in people living at higher latitudes (northern climates) and
in younger people.
Double Depression
• It is common for major depression to coexist with dysthymia
• Moderately depressed on a chronic basis (meeting symptom criteria for dysthymia) but
• undergo increased problems from time to time(meet criteria for a major depressive episode).
• More common in clinical samples of dysthymia than in people with dysthymic
disorder who never seek treatment.
• For ex, one clinical sample of nearly 100 individuals with early-onset dysthymia
(onset before age 21) was followed for 10 years, during which time 84% experienced
at least one major depressive episode.
• Although nearly all individuals with double depression appear to recover from their
major depressive episodes (although usually just to their previous level of
dysthymia) recurrence is common.
• “Persistent” – less pejorative than the word chronic.
Causal Factors in Unipolar Mood
unipolar Disorders
A number of different causal factors have been studied in context of the etiology of
mood disorder including
biological, psychological, and sociocultural factors. Biopsychosocial Model – interaction
Biological Causal
between these causal factors
Psychological Causal
factors factors
• Genetic influence • Stressful life events
• Neurochemical influence • Different vulnerabilities

• Neurohormonal factors and • Psychodynamic


immune system • Behaviouristic
• Neurophysiological and • Beck’s cognitive theory
neuroanatomical factors • Hopelessness and helplessness theory
• Sleep and biological rhythms • Rumination theory
Biological Factors
• There are many different approaches to understand the biological factors
underlying the development of unipolar mood disorders.
• Hippocrates hypothesized that depression was caused by an excess of black
bile (400 B.C.).
• Researchers have found the possible role of
1. genetics,
2. neurochemistry,
3. hormones,
4. neuroanatomy, neurophysiology,
5. sleep and circadian rhythms.
Genetics
• Family, twin, and adoption studies make a strong case for moderate genetic
contribution
• Family studies report that 2 to 3 times higher among blood relatives of persons
group.
• Severity, recurrence, earlier age of onset are associated with higher rates of depression in
relatives.
• Twin studies have also found higher concordance rate in MZ twins than DZ twins.
• Moreover, concordance rates are found to be higher for females than males.
• Adoption studies also provide support for genetic basis of unipolar mood
disorders; chances of unipolar depression were higher in biological relatives of
adopted children than in biological relatives of control-adopted children.
• Serotonin-transporter gene is involved in transmission and reuptake of serotonin.
• Serotonin transporter gene has two different kind of versions: the short allele (s) and the long
allele (I). For a person it can be (s/s), (l/l) or (s/l)
• (s/s) predisposes to depression
• Genotype-environment interaction.
• (s/s) alleles with four or more stressful life events
• (s/s) alleles with severe maltreatment in childhood
• No one faulty gene underlying depression – there are several
“pattern of genes.”
• Temperament of neuroticism that predisposes to both anxiety and
depression.
• Genetic factors may provide a diathesis for development of
depression.
• Faulty genes may produce neurochemical, neuroanatomical,
neurophysiological and hormonal changes.
Neurochemical Factors
• Neurotransmitter activities to play a role in depression.
• Monoamine hypothesis of depression presented in 1960s-70s
focused on serotonin and norepinephrine – involved in regulation of
behavioural activity, stress, emotional expression, and vegetative
function (appetite, sleep, arousal)
• Depression is a result of absolute or relative depletion of the one or
all of these neurotransmitters at important receptor sites in the
brain.
• Depletion is because of either: (1) reduced production, (2) increased
degradation of the neurotransmitters at the synapse, or (3) altered
functioning of the postsynaptic receptors.
• Follow up studies found some contrary evidence to the monoamine
hypothesis.
• First, an increase in norepinephrine especially in those with severe or
melancholic depression
• Second, only a minority of patients with depression that is, those with more
severe symptoms and suicidal ideas had reduced serotonin activity.
• Third, medicines immediately increase the availability of neurotransmitters,
but they take about 2-4 weeks to show effect.
• By 1980s, it was clear that a straightforward mechanism is not possible.
• Depression may be related to reduced sensitivity of post-synaptic
receptors for dopamine and serotonin levels.
• Serotonin in particular has been implicated in unipolar depression.
• People who are vulnerable to depression may have less sensitive serotonin
receptors.
• Dopamine dysfunction (reduced activity) plays a significant role in at
least some forms of depression, including depression with atypical
features and bipolar depression.
• Dopamine is so prominently involved in the experience of pleasure and
reward.
• Reduced sensitivity to dopamine is related to anhedonia (the inability to
experience pleasure), lack of motivation and energy.
• Most recent studies have focused on the interaction of
neurotransmitters, and hormones, brain activity, and biological rhythms.
Abnormalities of Hormonal Regulatory and Immune
Systems
• Dysregulation of HPA axis and HPT axis
• According to the stress hypothesis, people with depression have
dysfunction in the HPA axis leading to the increased blood plasma
levels of cortisol (stress hormone).
• Cortisol levels are poorly regulated in people with depression.
• Blood plasma cortisol levels elevated in 20%–40% of depressed
outpatients and 60%–80% of severely depressed hospitalized patients.
• Sustained elevations in cortisol—a “hallmark of mammalian stress
responses”—can result from increased CRH activation, increased
secretion of ACTH, or the failure of feedback mechanisms.
• Elevations in cortisol may be due to failure of feedback mechanisms—
dexamethasone.
• HPA axis is partly controlled by norepinephrine and serotonin.
• Elevated stress hormone (cortisol) levels are consistent with the
relationship between depression and severe stress.
• Recent evidence suggests that dexamethasone nonsuppression may be
a general indicator of mental distress rather than specific to
depression.
• Prolonged elevations of cortisol lead to
cell death in the hippocampus.
• High cortisol levels are harmful to neurons.
• Neurons in hippocampus are affected
leading to problems with memory
impairments and problems with abstract
thinking.
• Hippocampus also keeps regulating cortisol.
• Low hippocampal neuronal volume
precedes and contributes to onset of
depression.
• About 40-60 % of depressed patients show dysregulation of the
Hypothalamic-Pituitary- Thyroid (HPT) axis.
• 20%–30% of depressed people who have normal thyroid
functioning show dysregulation in this axis.
• Using drugs to increase thyroid hormone levels can lower
depression in these individuals.
• Hypothyroidism, which is low levels of thyroid, is often discovered.
Neurophysiological and Neuroanatomical
Influences
• Damage (for example, from a stroke) to the left, but not
the right, anterior prefrontal cortex often leads to
depression
• Lowered levels of brain activity in left anterior
prefrontal cortex
• The electroencephalographic (EEG) activity of both
cerebral hemispheres in people who are depressed,
shows an asymmetry or imbalance in the EEG activity
of the two sides of the prefrontal regions of the brain.
• low activity in the left hemisphere in these regions and
relatively high activity in the right hemisphere
• lower activity on the left side of the prefrontal cortex – reduced
positive affect and reduced approach behaviors to rewarding
stimuli
• increased right-side activity – increased anxiety symptoms and
increased negative affect, increased vigilance for threatening
information
• Several regions: orbital prefrontal cortex, dorsolateral prefrontal
cortex, hippocampus, anterior cingulated cortex, and the
amygdala have all been shown to play a role in depression.
• Decreased volume of orbital prefrontal cortex - reduced responsivity to
reward
• Lower levels of activity in the dorso lateral prefrontal cortex – decreased
cognitive control
• Decreased volume and abnormally low levels of activation in anterior
cingulate cortex – affects selective attention (inability to prioritize important
info), affects self-regulation and adaptability
• Increased activity of amygdala (perception of threat and in directing
attention) – biased attention to negative emotional information.
• Prolonged depression often leads to decreased hippocampal
volume
Sleep and Other Biological
Rhythms
• Sleep – 5 stages that occur in a relatively invariant
sequence throughout the night
• Stages 1 to 4 of non-REM sleep and REM sleep make
up a sleep cycle.
• REM sleep is characterized by rapid eye movements
and dreaming as well as other bodily changes;
• First REM period is about 75 to 80 minutes into sleep.
• Normal sleep–wake cycle is regulated by the
hypothalamus
• Patients who are depressed often show one or more of a variety of sleep problems
• difficulty falling asleep
• periodic awakening during the night (poor sleep maintenance)
• early morning awakening,

1. Many enter the first period of REM sleep after only 60 minutes or less of sleep (i.e., 15 to 20
minutes sooner)
• Greater amounts of REM sleep during the early cycles
• Intensity and frequency of REM are also greater
2. Lower-than-normal amount of deep sleep (Stages 3 and 4).
• Precede the onset of depression and persist following recovery
• May be vulnerability markers for certain forms of major depression
• Humans have many circadian (24-hour, or daily) cycles other than sleep, including body
temperature, propensity to REM sleep, and secretion of cortisol, thyroid-stimulating hormone,
and growth hormone.
• Research has found some abnormalities in all of these rhythms in patients with depression
• The various circadian rhythms that are normally well synchronized with each other become
desynchronized or uncoupled
Sunlight and Seasons
• Abnormality or disturbance in circadian rhythm is seen in seasonal
affective disorder
• They are responsive to the total quantity of available light in the environment
• A majority become depressed in the fall and winter and normalize in
the spring and summer
• Research in animals has also documented that many seasonal
variations in basic functions such as sleep, activity, and appetite are
related to the amount of light in a day (which, except near the
equator, is much greater in summer than in winter).
• SAD show increased appetite and hypersomnia rather than
decreased appetite and insomnia
• Clear disturbances in their circadian cycles, showing weaker 24-hour
patterns
• Treatment to SAD – a controlled exposure to light, even artificial
light, which may work by reestablishing normal biological rhythms.
• Although anti-depressant medications can also be useful, the use of
light therapy is more cost efficient in the long term
• Biological explanation for sex difference
For females, hormones play a crucial role with the onset of puberty,
before menstrual cycles, postpartum period, and menopause.
Women have a greater genetic predisposition.
• Summary of biological causal factors
Moderate genetic contribution is mediated by environmental
factors.
Stress response system is chronically overactivated.
Severe depression is linked to multiple interacting disturbances in
neurochemical, neuroendocrine, and neurophysiological systems.
Those with less severe depressions may show few, if any,
biological abnormalities.
Psychological Causal Factors
• Stressful life events • Cognitive theory –
• Mildly stressful events and chronic Beck
stress
• Evaluating Beck’s
• Vulnerability and response to theory
stresses
• Different types of vulnerabilities • Helplessness theory
• Personality diathesis • Hopelessness theory
• Cognitive diathesis • Rumination style
• Early adversity theory
• Psychodynamic theories
• Behavioural theories
Stressful Life Events as Causal Factors

• Severely stressful life events often serve as precipitating factors


for unipolar depression.
• Like loss of a loved one,
• serious threats to important close relationships or to one’s occupation,
or
• severe economic or serious health problems,
• separations through death or divorce
• Losses that involve an element of humiliation can be especially
potent.
• The stress of being the caregiver to a spouse with a debilitating
disease such as Alzheimer’s is also known to be associated with
the onset of both MDD and GAD in the caregiver
• Stronger for young female adults than in men
Independent Life events Vs Dependent Life events
• Independent of the person’s behavior and personality - such as losing a job because
one’s company is shutting down or having one’s house hit by a hurricane
• Events that may have been at least partly generated by the depressed person’s behavior
or personality.
• Dependent life events play a stronger role in the onset of MDD
• For ex, people with depression sometimes generate stressful life events through their
poor interpersonal problem solving (such as being unable to resolve conflicts with a
spouse).
• Poor problem solving – higher levels of interpersonal stress – depression.
• Another ex of a dependent life event is failing to keep up with routine tasks such as
paying bills, which may lead to a variety of troubles.
• Minor events may play more of a role in the onset of recurrent episodes than in the
initial episode.
• Living in poverty and chronic stress can increase vulnerability
• Some are more vulnerable: Women (and perhaps men) at genetic risk for depression not
only experience more stressful life events
Different types of
Vulnerabilities
Personality Diathesis
• An individual high on the personality trait of neuroticism or
negative affectivity– vulnerable to unipolar depression.
• They tend to be sensitive to a broad range of negative moods including
sadness, guilt, anxiety, hostility etc.
• Neuroticism predicts the occurrence of more stressful life
events,
• Poorer prognosis
• High levels of introversion (or low positive affectivity) may also
serve as vulnerability factors for depression, either alone or
when combined with neuroticism
Cognitive Diathesis
• Pessimistic attributional style
• Cognitive diatheses that have been studied for depression
generally focus on particular negative patterns of thinking
that make people who are prone to depression more likely
to become depressed when faced with one or more
stressful life events.
• For ex, people who attribute negative events to internal
(my fault), stable (always going to happen), and global
(affects everything in my life)causes may be more prone to
becoming depressed than are people who attribute the
same events to external, unstable, and specific causes.
• Ex. ;
• Low grade – I am stupid (pessimistic depressive style)
• Teacher deliberately wrote a difficult test to make us all realize we
need to study harder. (optimistic attribution)
• A range of adversities in the early environment such as
• family turmoil, parental psychopathology, physical or sexual abuse, and
other forms of intrusive, harsh, and coercive parenting can create both
a short-term and a long-term vulnerability to depression.
• Parental loss followed by poor care
• Increases an individual’s sensitivity to stressful life events in adulthood
• Low self-esteem and insecure attachment with a caregiver.
• Can lead to “stress inoculation” if adversity is moderate rather than severe and
mediated by strengthening socio-emotional and neuroendocrine resistance
• Long-term effects of such early environmental adversities may be
mediated by both
• biological variables (such as alterations in the regulation of the HPA stress
response system) and
• psychological variables (such as lower self-esteem, insecure attachment
relationships, difficulty relating to peers, and pessimistic attributions)
Psychodynamic Theories
• Freud - depression is in response to imagined or symbolic losses.
• Freud - similarity between the symptoms of clinical depression and the symptoms
seen in people mourning the loss of a loved one.
• Freud and a colleague, Karl Abraham (1927), both hypothesized that when a loved
one dies the mourner regresses to the oral stage of development (when the infant
cannot distinguish self from others) and introjects or incorporates the lost person,
feeling all the same feelings toward the self as toward the lost person.
• These feelings include anger and hostility because Freud believed that we
unconsciously hold negative feelings toward those we love, in part because of
their power over us.
• Depression is anger turned inward.
• For ex, a student who fails in school or who fails at a romantic relationship may
experience this symbolically as a loss of his or her parents’ love.
Behavioural Theories
• People become depressed either
• when their responses no longer produce positive reinforcement or
• when their rate of negative experiences increases (such as when experiencing stressful life
events)
• People with depression –
• fewer positive verbal and social reinforcements from their families and friends
• experience more negative events
• lower activity levels, and
• their moods seem to vary with both their positive and their negative experiences rates
• Certain primary symptoms, such as pessimism and low levels of energy, –
experiences lower rates of reinforcement – maintains depression.
• Not very influential as an etiological theory.
Beck’s Cognitive Theory
• Aaron Beck
• Cognitive symptoms of depression, (for ex, “I’m hopeless, total
failure”) precede and cause the affective symptoms of depression
(for ex, upset and miserable).
• Dysfunctional/depressogenic beliefs that are rigid, extreme
and counterproductive are formed during early childhood
through interactions with parents and significant others
• for ex, “I must be perfect in everything”, “I’m unworthy of being loved.
• These beliefs lie dormant (below the surface level of
awareness)and form a cognitive diathesis – later develop to
depression.
• These beliefs are never challenged and become self-fulfilling.
• For instance, a person who has a core belief that they are unworthy of
being loved may reject loving advances of others and may withdraw from
others making others reject in turn.
• Stressful life situations (called critical incidents), such as those involving
humiliation, loss, and social rejection, these dormant beliefs may become
dominant and may generate automatic negative thoughts.
• These are negative and pessimistic predictions about one’s self (I’m a
loser), others (nobody loves me), and future (it’s all hopeless, nobody
will ever love me).
• Beck labeled this as cognitive triad.
Negative cognitive triads are maintained by a variety of negative cognitive
biases or errors
Ex include:
• Dichotomous or all-or-none reasoning – tendency to think in extremes.
For ex, someone might discount a less-than-perfect performance by saying, “If I
can’t get it 100 percent right, there’s no point in doing it at all.”
• Selective abstraction – tendency to focus on one negative detail of a
situation while ignoring other elements of the situation.
For ex, Someone might say, “I didn’t have a moment of pleasure or fun today” not
because this is true but because he or she selectively remembers only the negative
things that happened.
• Arbitrary inference – jumping to a conclusion based on minimal or no
evidence.
For ex., A depressed person might say, after an initial homework assignment from
a cognitive therapist did not work, “This therapy will never work for me.”
• Each of these cognitive distortions maintain the negative cognitive triad.
• Contents of your thoughts regarding your views of your self, your world, and
your future is already negative.
• minimize the good things that happen to you or
• draw negative conclusions based on minimal evidence,
• those negative thoughts are not likely to disappear.
• Underlying dysfunctional beliefs elicit the negative cognitive triad when
activated
• Negative cognitive triad leads to negative thinking which in turn reinforce
those underlying beliefs.
• Also negative thoughts produce some other symptoms such as sadness,
dejection, and lack of motivation.
• Automatic negative thoughts can cause depressed mood and depressed
mood in turn can make negative thoughts salient,
• The ‘vicious cycle of depression.’
Evaluating Beck’s Theory as a Descriptive Theory
• Cognitive therapy - A very effective form of treatment for depression
• A descriptive theory that explains many prominent characteristics of depression
• Patients with depression of all the subtypes are considerably more negative in their
thinking, especially about themselves or issues highly relevant to the self,
• People who are not depressed show a tendency to process emotional information in an
overly optimistic, self enhancing manner, which may serve as a protective factor
against depression
• Beck’s theory originally proposed that stressors are necessary to activate
depressogenic schemas or dysfunctional beliefs that lie dormant between episodes,
• But more recent research has shown that stressors are not necessary to activate the
latent depressive schemas between episodes.
• Indeed, simply inducing a depressed mood (e.g., through listening to sad music or
recalling sad memories) in an individual who was previously depressed (that is, at risk)
is generally sufficient to activate latent depressogenic schemas
• Evidence for dysfunctional beliefs and negative automatic
thoughts,
• Evidence for certain cognitive biases for negative self-relevant
information in depression.
• For ex, people with depression show better or biased recall of negative
information and negative autobiographical memories,
• people who are not depressed tend to show biased recall of positive
emotional information and positive autobiographical memories.
• People with depression are more likely
• to draw negative conclusions that go beyond the information presented in
a scenario and to underestimate the positive feedback they have received.
• Already depressed – remembering the bad things that have
happened – maintains depression
• Teasdale (1988, 1996) aptly called this the “vicious cycle of
depression.”
Helplessness Theory of
Depression
• Martin Seligman first proposed that the laboratory phenomenon
known as learned helplessness might provide a useful animal
model of depression.
• It states that when animals or humans find that they have no
control over aversive events (such as shock), they may learn that
they are helpless, which makes them unmotivated to try to
respond in the future.
• Instead they exhibit passivity and even depressive symptoms.
• Learned helplessness may underlie some types of human
depression.
• That is, people undergoing stressful life events over which they
have little or no control may develop a syndrome like the
helplessness syndrome seen in animals.
Reformulated Helplessness Theory

• Abramson and colleagues


• When people are exposed to uncontrollable negative events, they ask
themselves why, and the kinds of attributions that people make are,
in turn, central to whether they become depressed.
• These investigators proposed three critical dimensions on which
attributions are made:
(1) internal/external, (2) global/specific, and (3) stable/unstable.

• Depressogenic or pessimistic attribution for a negative event is


internal, stable, and global.
• For ex, if your boyfriend treats you badly and you conclude that “It’s because
I’m ugly and boring,” you are much more likely to become depressed than if you
conclude that “It’s because he’s in a bad mood today and he is taking it out on
me.”
• Abramson and colleagues (1978) proposed that people who have
a relatively stable and consistent pessimistic attributional style
have a vulnerability or diathesis for depression when faced with
uncontrollable negative life events.
• This kind of cognitive style seems to develop through social
learning.
• For ex, children may learn this cognitive style by observing and modeling
inferences made by their parents.
• The parents may communicate their own inferences about negative
events happening to their children
• Engage in generally negative parenting practices such as high levels of
negative psychological control (criticism, intrusiveness, and guilt) as well
as a lack of warmth and caring.
Helplessness theory can explain sex differences in depression.
• By virtue of their roles in society, women are more prone to experiencing
a sense of lack of control over negative life events.
• These feelings of helplessness might stem from
• poverty,
• discrimination in the workplace leading to unemployment or underemployment,
• the relative imbalance of power in many heterosexual relationships,
• high rates of sexual and physical abuse against women (either currently or in childhood),
• role overload (e.g., being a working wife and mother), and
• less perceived control over traits that men value when choosing a long-term mate, such
as beauty, thinness, and youth.
• Women have higher levels of neuroticism and experience more uncontrollable
stress,
• Thus, the increased prevalence of depression in women becomes less
surprising
Hopelessness Theory of Depression
• Abramson and colleagues propose that having a pessimistic attributional style in
conjunction with one or more negative life events was not sufficient to produce
depression unless one first experienced a state of hopelessness.
• A hopelessness expectancy
• The perception that one had no control over what was going to happen and
• by the absolute certainty that an important bad outcome was going to occur
• or that a highly desired good outcome was not going to occur.
• They also proposed that the internal/external dimension of attributions was not
important to depression.
• Instead, they propose two other dimensions of pessimistic attributional style (global
and stable) as being important components of this cognitive diathesis.
• tend to make negative inferences about other likely negative consequences of the event
(e.g., that this means more bad things will also happen) and
• negative inferences about the implications of the event for the self-concept (e.g., that one is
unworthy or deficient;)
• Integrate hopelessness theory with a
motivational theory of depression
• Depression is associated with decreased
approach behavior.
• Cognitively vulnerable individuals are at risk
• for decreased approach-related behavior as a
result of increased hopelessness under stress,
thereby contributing to depression.
The Ruminative Response Styles Theory
• Nolen-Hoeksema’s ruminative response style cognitive theory of depression
• focuses on different kinds of responses that people have when they experience feelings and
symptoms of sadness and distress,
• and how it affect the course of their depressed feelings.
• Some people tend to focus intently on how they feel and why they feel that way—a
process called rumination, which involves a pattern of repetitive and relatively
passive mental activity.
• Other people, have a more action-oriented or problem-solving response to such
feelings and, for ex,
• distract themselves with another activity or
• actually try to do something that will solve the problems that are leading to the sadness and
distress.
• There are stable individual differences in the tendency to ruminate
• People who ruminate a great deal tend to have more lengthy periods
of depressive symptoms.
• More likely to develop full-blown episodes of MDD
• Women are more likely than men to ruminate when they become
depressed
• Self-focused rumination leads to increased recall of more negative
autobiographical memories – a vicious circle of depression
• Men are more likely to engage in a distracting activity (or consume
alcohol) when they get in a depressed mood, and distraction seems to
reduce depression
• Distraction might include going to a movie, playing a sport, or avoiding thinking
about why they are depressed.
• Effective prevention efforts might include teaching girls to seek
distraction rather than to ruminate as a response to depression.
• In short,
• People with high levels of dysfunctional attitudes
and/or pessimistic attributional styles, their
tendencies to ruminate moderated the effects of
the negative cognitive styles on increasing
vulnerability to depression.
• Specifically, those who had negative cognitive
styles who also tended to ruminate a lot were
most likely to develop depressive episodes.
• The researchers suggest that people with
negative cognitive styles have a lot of negative
content to their thoughts but that only if they
dwell on this and brood about it (high
ruminators) are they especially likely to develop
clinical depression.
Interpersonal Effects of Mood
Disorders
• Considerable amount of research on
interpersonal factors in depression.
• Interpersonal problems and social-skills
deficits may well play a causal role in at
least some cases of depression.
• In addition, depression creates many
interpersonal difficulties—with
strangers and friends as well as with
family members
Lack of Social Support and Social-Skills Deficits
• Women without a close, confiding relationship were more likely to
become depressed if they experienced a severely stressful event.
• People who are lonely, socially isolated, or lacking social support
are more vulnerable to becoming depressed
• In addition, some people with depression have social-skills deficits.
• For example, they seem to speak more slowly and monotonously and to
maintain less eye contact;
• they are also less skilled than people at solving interpersonal problems
• their own behavior also seems to make these problems worse.
• Depressive behavior can, and over time frequently does, elicit
negative feelings (sometimes including hostility) and rejection in
other people, including strangers, roommates, and spouses.
• Social rejection may be especially likely if the person with
depression engages in excessive reassurance seeking.
Marriage and Family Life
• Interpersonal aspects of depression have also been carefully
studied in the context of marital and family relationships.
• A significant proportion of couples experiencing marital distress
have at least one partner with clinical depression, and there is a
high correlation between marital dissatisfaction and depression
for both women and men.
• In addition, marital distress spells a poor prognosis for a spouse
with depression whose symptoms have remitted.
• That is, a person whose depression clears up is likely to relapse if he or
she has an unsatisfying marriage, especially one characterized by high
levels of critical and hostile comments from the spouse.
• Criticism is associated with relapse in depression because it is
capable of activating some of the neural circuits involved in the
disorder.
• People who are vulnerable to depression may be especially
sensitive to criticism even after they have made a full recovery.
• Marital distress and depression may co-occur because the depressed
partner’s behavior triggers negative affect in the spouse.
• Individuals with depression may also be so preoccupied with
themselves that they are not very sensitive or responsive to the needs
of their spouses.
• The effects of depression in one family member extend to children
of all ages.
• Parental depression puts children at high risk for many problems, but
especially for depression.
• Effect of maternal depression is larger
• Children tend to become depressed earlier and to show a more severe
and persistent course
• Children inherit a variety of traits such as temperament (including
shyness, behavioral inhibition, and neuroticism), low levels of positive
emotions, and poor ability to regulate emotions that are all known
risk factors for depression
• Damaging effects of negative interactional patterns
between mothers with depression and their children.
• For ex, mothers with depression show more friction and have
fewer playful, mutually rewarding interactions with their
children.
• Less sensitively attuned to their infants and less affirming of
their infants’ experiences.
• Their young children are given multiple opportunities for
observational learning of negative cognitions, depressive
behavior, and depressed affect.
• Thus, although genetically determined vulnerability is
clearly involved, psychosocial influences clearly also play
an important role, and
• evidence is accumulating that inadequate parenting is
what mediates the association between parental
depression and their children’s depression
Bipolar and Related
Disorders

• Bipolar disorders are distinguished from unipolar disorders by


the presence of manic or hypomanic episodes, which are
nearly always preceded or followed by periods of depression.
Manic episode
• Markedly elevated, euphoric, or expansive mood,
• often interrupted by occasional outbursts of intense irritability or even violence—
particularly when others refuse to go along with the manic person’s wishes and
schemes.
• These extreme moods must persist for at least a week for diagnosis
• In addition, three or more additional symptoms must occur in the same time
period, ranging from
• behavioral symptoms (such as a notable increase in goal-directed activity,
• mental symptoms where self-esteem becomes grossly inflated and mental activity may speed
up (such as a “flight of ideas” or “racing thoughts”),
• physical symptoms (such as a decreased need for sleep or psychomotor agitation).
• During the period of mood disturbance and increased energy or activity, 3 (or
more) of the following symptoms (four if the mood is only irritable) are
present to a significant degree and represent a noticeable change from usual
behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant
external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or
sexually) or psychomotor agitation (i.e., purposeless non-goal-directed activity).
7. Excessive involvement in activities that have a high potential for painful
consequences (e.g., engaging in unrestrained buying sprees, sexual
indiscretions, or foolish business investments).
Hypomanic Episode
• Similar symptoms in milder forms
• Person experiences abnormally elevated, expansive, or irritable mood for at
least 4 days.
• At least 3 other symptoms similar to those involved in mania but to a lesser
degree
• e.g., inflated self-esteem,
• decreased need for sleep,
• flights of ideas,
• pressured speech, etc.
• Less impairment in social and occupational functioning in hypomania,
• Hospitalization is not required.
Cyclothymic Disorder
• Cyclical mood changes less severe than the mood swings seen
in bipolar disorder.
• Historically these were referred to as cyclothymic
temperament.
• Persist for at least 2 years
• In DSM-5, cyclothymia is defined as a less serious version of
full-blown bipolar disorder because it lacks
• certain extreme symptoms and psychotic features such as delusions
and
• the marked impairment caused by full-blown mania or major
depression
• Depressed phase of cyclothymic disorder, • Hypomanic phase of
• Similar to dysthymia except duration cyclothymia
criteria • Opposite of the symptoms of
• a person’s mood is dejected, dysthymia.
• a distinct loss of interest or pleasure in • Especially creative and
customary activities and pastimes.
productive because of
• low energy, increased physical and mental
• feelings of inadequacy, energy.
• social withdrawal,
• pessimistic,
• There brooding
may be significant attitude.
periods between episodes in which functions in a relatively
adaptive manner.
• at least a 2-year span during which there are numerous periods with hypomanic and
depressed symptoms
• 1 year for adolescents and children
• the symptoms must cause clinically significant distress or impairment in functioning
(although not as severe as in bipolar disorder).
• Increased risk of later developing full-blown bipolar I or II disorder.
• Clinical attention recommended.
• Kraepelin, in 1899, introduce the term manic-depressive insanity
• Kraepelin described the disorder as a series of attacks of elation and
depression, with periods of relative normality in between.
• Bipolar I disorder
• Bipolar II disorder
Bipolar I Disorder
• Distinguished from major depressive disorder by the
presence of mania or a mixed episode
• A mixed episode – symptoms of both full-blown manic and
major depressive episodes for at least 1 week, whether the
• symptoms are intermixed or alternate rapidly every few days.
• Such cases are relatively common
• Moreover, many patients in a manic episode have some
symptoms of depressed mood, anxiety, guilt, and suicidal
thoughts, even if these are not severe enough to qualify as a
mixed episode.
• a person shows only manic symptoms, it is nevertheless
assumed that a bipolar disorder exists and that a depressive
episode will eventually occur.
Bipolar II disorder

• Experience clear-cut hypomanic


episodes and major depressive
episodes
• Bipolar II disorder is equally or
somewhat more common than
bipolar I disorder
• In 5-15% cases evolves into bipolar I
disorder
• Bipolar disorder occurs equally in males and females
• usually starts in adolescence and young adulthood,
• with an average age of onset of 18 to 22 years
• Bipolar II disorder – onset approximately 5 years later than bipolar I disorder
• Both bipolar I and II are typically recurrent disorders, with people
experiencing single episodes extremely rarely.
• In about 2/3 of cases, the manic episodes either immediately precede or
immediately follow a depressive episode;
• in other cases, the manic and depressive episodes are separated by intervals of
relatively normal functioning.
• Periods of remission and symptom free
• Majority have chronic occupational or interpersonal problems between
episodes.
• As with unipolar major depression, the recurrences can be seasonal in nature,
• bipolar disorder with a seasonal pattern is diagnosed.
Features of Bipolar Disorder
• Duration of manic and hypomanic episodes tends to be shorter than the duration of
depressive episodes,
• 3 times as many days spent depressed as manic or hypomanic
• Can you distinguish symptoms of depression in unipolar and bipolar?
• High degree of overlap in symptoms but there are some significant differences.
• In bipolar – more mood lability, psychotic features, psychomotor retardation, and more substance abuse.
• In unipolar – more anxiety, agitation, insomnia, physical complaints, and weight loss.
• Bipolar – more severe depression, more impairment
• Suicide attempts may be more common in bipolar than in unipolar
• For diagnosis of bipolar I patient must show at least one manic or mixed episode in
the past.
• Many people with bipolar disorder whose initial episode or episodes are depressive
are misdiagnosed at first and possibly throughout their lives (for instance, if no manic
episodes are observed or reported, or if they die before a manic episode is
experienced).
• Misdiagnoses are unfortunate because
• different treatments for unipolar and bipolar depression.
• Some antidepressant drugs used to treat unipolar depression may actually
precipitate manic episodes in patients who actually have as-yet-undetected
bipolar disorder, thus worsening the course of the illness
• Younger the person is at the time of the first diagnosis, and the
greater the number of recurrent episodes, the more likely
diagnosed with bipolar.
• People presenting initially with a MDD who have a history of
creative achievements, professional instability, multiple marriages,
and flamboyant behavior may be especially likely to be diagnosed
later with bipolar II disorder
Rapid Cycling
• Suffer more episodes during their lifetimes than with unipolar disorder (although
shorter episodes - 3 to 4 mths).
• Some experience at least four episodes (either manic or depressive) every year,
a pattern known as rapid cycling.
• In fact, those who go through periods of rapid cycling usually experience many
more than four episodes a year.
• Rapid cycling are slightly more in women,
• to have a history of more episodes (especially more manic or hypomanic episodes),
• to have an earlier onset, and
• to make more suicide attempts.
• Precipitated by taking certain kinds of antidepressants.
• Fortunately, for about 50 % of cases, rapid cycling is a temporary phenomenon
• Gradually disappears within about 2 years
• Probabilities of “full recovery” from bipolar disorder are
discouraging even with the widespread use of mood-stabilizing
medications such as lithium,
• About 20 % of their lives in episodes.
• One 20-year prospective study in which over 200 patients were
followed for an average of 17 years found that
• 24 % relapsed within 6 months of recovery;
• 77 % at least one new episode within 4 years of recovery
• 82 % relapsed within 7 years.

• More severe for patients who have comorbid substance-abuse


or dependence disorders.
Causal Factors in Bipolar
Disorders
• As for unipolar disorders, a host of causal
factors for bipolar disorder have been
posited over the past century.
• However, biological causal factors are
clearly dominant, and
• the role of psychological causal factors
has received significantly less attention.
Biological Causal Factors
• A number of biological factors are thought to play a causal
role in the onset of bipolar disorder.
• These factors include
• genetic,
• neurochemical,
• hormonal,
• neurophysiological, neuroanatomical, and
• biological rhythm influences.
Genetic Influences
• Higher heritability than unipolar or any of the other major adult
psychiatric disorders, including schizophrenia.
• Family studies and twin studies
• Higher concordance for identical twins
• Greater genetic contribution to bipolar I disorder than in unipolar
disorder.
• First-degree relatives of a person with bipolar I illness can be
expected to have bipolar disorder
• They are also at elevated risk for unipolar major depression (especially
atypical depression), although the reverse is not true
• Genetic influences are even stronger in early- as opposed to late-
onset bipolar disorder
• Efforts to locate the chromosomal site(s) of the implicated gene or
genes in this genetic transmission of bipolar disorder suggest that it
is polygenic.
Neurochemical Factors
• Norepinephrine, serotonin, and dopamine are all involved in
regulating our mood states.
• Monoamine hypothesis extended to bipolar disorder
• if depression is caused by deficiencies of norepinephrine or serotonin, then mania is
caused by excesses of these neurotransmitters.
• Increased norepinephrine activity during manic episodes and less
consistent evidence for lowered norepinephrine activity during depressive
episodes.
• Serotonin - low in both depressive and manic phases.
• Increased activity of dopamine – manic symptoms of hyperactivity,
grandiosity, and euphoria.
• High doses of drugs such as cocaine and amphetamines, which are
known to stimulate dopamine, also produce manic-like behaviour.
• Drugs like lithium reduce dopaminergic activity and are anti-manic.
• In depression there appear to be decreases in both norepinephrine and
dopamine functioning.
Abnormalities of Hormonal Regulatory
Systems
• Dysfunctions in HPA and HPT axis.
• Cortisol levels are elevated in bipolar
depression (as they are in unipolar depression),
but they are usually not elevated during manic
episodes.
• Abnormalities of thyroid function are frequently
accompanied by changes in mood.
• Administration of thyroid hormone often makes
antidepressant drugs work better.
• However, thyroid hormone can also precipitate
manic episodes in patients with bipolar disorder
Neurophysiologic and Neuroanatomic
Influences
• Positron emission tomography (PET) scans – visualize variations in brain glucose metabolic rates in
depressed and manic states,
• great difficulties studying patients who are actively manic.
• Shifting patterns of brain activity during mania and during depressed and normal moods.
• Reduced blood flow to the left prefrontal cortex is reduced during depression,
• Increased activity prefrontal cortex during mania
• Deficits in activity in the prefrontal cortex
• Show neuropsychological deficits – problem solving, planning, working memory, shifting of attention, and sustained
attention on cognitive tasks.
• Deficits in the anterior cingulate cortex (in unipolar too)
• Basal ganglia and amygdala are enlarged in bipolar disorder but reduced in size in unipolar depression.
• fMRI – increased activation in thalamus and amygdala (emotional processing)
• Dysregulation in frontal-limbic activation .
• The decreases in hippocampal volume that are often observed in unipolar depression are generally not
found in bipolar depression.
• Hopefully more definitive findings will follow when much-needed technological innovations unfold
Sleep and Other Biological
Rhythms
• Disturbances in biological rhythms such as circadian rhythms,
even after symptoms have mostly remitted
• During manic episodes – tend to sleep very little (seemingly by
choice, not because of insomnia), and this is the most common
symptom to occur prior to the onset of a manic episode.
• During depressive episodes, they tend toward hypersomnia (too
much sleep).
• Even between episodes – substantial sleep difficulties, including
high rates of insomnia.
• Disturbances of seasonal biological rhythms, although these may
be the result of circadian abnormalities in which the onset of the
sleep–wake cycle is set ahead of the onset of other circadian
rhythms.
• Especially sensitive to, and easily disturbed by, any changes in
their daily cycles that require a resetting of their biological clocks.
Psychological Causal Factors
• Although biological factors play a prominent role in the onset of
bipolar disorder, psychosocial factors have also been found to be
involved in the etiology of the disorder. In particular,
• stressful life events,
• poor social support, and
• certain personality traits and
• cognitive styles
have been identified as important psychological causal
factors.
Stressful Life Events
• Important in precipitating bipolar depressive episodes.
• Sometimes precipitates even manic episodes.
• Influences the timing of an episode, by activating the underlying
vulnerability.
• Severe negative events took an average of three times longer to
recover from manic, depressive, or mixed episodes (395 versus 112
days).
• Even minor negative events were found to increase time to recovery.
• As the illness unfolds, the manic and depressive episodes become
more autonomous and do not usually seem to be precipitated by
stressful events.
• Some of these conclusions may be premature
relied on patients’ memories of events before episodes, which may be unreliable.
Other Psychological Factors
• Other social environmental variables may also affect the course of bipolar
disorder.
• low social support showed more depressive recurrences over a 1-year follow-up,
independent of the effects of stressful life events, which also predicted more
recurrences.
• There is also some evidence that personality and cognitive variables may
interact with stressful life events in determining the likelihood of relapse.
• neuroticism
• Personality variables and cognitive styles that are related to goal-striving, drive,
and incentive motivation.
• high levels of achievement striving and increased sensitivity to rewards in
the environment predicted increases in manic symptoms—especially during
periods of active goal striving or goal attainment (such as studying for an
important exam and then doing very well in it).
• a pessimistic attributional style who also had negative life events showed an
increase in depressive symptoms and manic symptoms
Sociocultural factors affecting
mood disorders
• Cross-Cultural Differences in Depressive
Symptoms
• China and Japan—psychological symptoms of depression are
low; somatic and vegetative manifestations are higher.
• Indian – high prevalence of physical and somatic symptoms
• Complaints of body ache and vague pain
• As Asian cultures have incorporated Western values, rates
of depression have increased.
• Adolescents from Hong Kong were shown to have higher
rates of depression than adolescents in the United States.
• Several possible reasons for these symptom differences stem from Asian beliefs
in the unity of the mind and body, a lack of expressiveness about emotions
more generally, and the stigma attached to mental illness in these cultures.
• Another reason why guilt and negative thoughts about the self may be common
in Western but not in Asian cultures is that Western cultures view the individual
as independent and autonomous, so when failures occur, internal attributions
are made.
• By contrast, in many Asian cultures individuals are viewed as inherently
interdependent with others.
• Nevertheless, as countries like China have incorporated some Western values
over the course of becoming increasingly industrialized and urbanized, rates of
depression have risen a good deal relative to several decades ago.
• Cross-Cultural Differences in Prevalence
• Varies tremendously; Taiwan—1.5%, whereas United
States and Lebanon—17% to 19%
• Need to identify risk factors in each culture
• Depression occurs in all cultures however the form of depression and prevalence rates
are different from culture to culture. Higher rates of depression have been seen in
western/westernized cultures. In cultures like China and Japan the rates of depression
are low and the psychological symptoms of depression may not show (guilt, pessimistic
attributions, hopelessness), instead somatic/vegetative symptoms (aches and pains,
lack of energy, sleep and eating disturbances) may be more prominent. This may be
because in individualistic cultures, the self is viewed as independent and autonomous.
In face of failures in individualistic cultures, internal attributions are made. Whereas
in collectivistic cultures, there is reciprocity between culture and individual and when
loss occurs, most likely it is made sure that hopelessness and helplessness do not set
in an individual. Also, even where psychological symptoms may be present, somatic
symptoms may be given more legitimacy because stigma attached to mental illness
and because of the belief in the unity of the mind and body.
• Socio Economic Status (SES) has been found to be inversely proportional
to depression. This may be because low SES leads to increased life
adversity and stress. Whereas, bipolar disorder is more common in
higher SES possibly because the personality and behavioural correlates
of bipolar illness in hypomanic phases (outgoingness, increased energy,
and increased productivity) may lead to increased achievements and
accomplishments. Many famous poets, writers, composers, and artists
have been found to have bipolar disorder. It has been proposed that
either, hypomania facilitates creative processes (for example,Vincent Van
Gough) or that intense negative emotional experiences of depression
provide material for creative activity (for example, Sylvia Plath).
Treatments and Outcomes
• Many patients who suffer from mood disorders
(especially unipolar disorders) never seek
treatment.
• Even without formal treatment, the great
majority of individuals with mania and depression
will recover (often only temporarily) within less
than a year.
• However, given the enormous amount of personal
suffering and lost productivity and given the wide
variety of treatments that are available today,
more and more people are seeking treatment.
• Severe unipolar depression and bipolar disorder
receive more treatment.
Alternative
Pharmacotherap
Biological Psychotherapy
y
Treatments
• MAOIs • ECT • CBT
• Tricyclics • TMS • Behavioural
• SSRIs • Deep Brain activation
• Lithium based Stimulation treatment
• Bright Light • Interpersonal
Therapy therapy
• Family and
Marital
therapy
Pharmacotherapy
• Antidepressant, mood-stabilizing, and antipsychotic drugs are all used in the
treatment of unipolar and bipolar disorders
• The first category of antidepressant medications was developed in the 1950s;
• These medications are known as monoamine oxidase inhibitors (MAOIs)
because they inhibit the action of monoamine oxidase – an enzyme responsible
for the breakdown of norepinephrine and serotonin once released.
• increasing availability of norepinephrine and serotonin
• Fatal Side effects with certain foods rich in amino acid tyramine
• Used only when other medications fail
• Depression with atypical features
Tricyclic anti- depressants
• For dysthymia and other depressive disorders
• Increase transmission of norepinephrine, to a lesser
extent serotonin
• Side Effects : dry mouth, constipation, sexual dysfunction,
and weight gain may occur which diminishes
• Many do not continue medication; to have its effect
• Cannot prescribe to suicidal patients: large doses highly
toxic: OD
Selective serotonin reuptake inhibitor (SSRI)
• fewer side effects
• better tolerated by patients
• less toxic in large doses.
• Side effect: problems with orgasm and lowered interest in sexual
activity, insomnia, increased physical agitation, and gastrointestinal
distress
• Also given to mild symptoms.
• Prescribing drugs to essentially healthy people merely because the
drugs make them feel more energetic, outgoing, and productive raises
many ethical questions.
Course of Treatment with
Antidepressant Drugs
• At least 3 to 5 weeks to take effect
• No signs of improvement after about 6 weeks, physicians try a new medication
• 50 % will respond to a second one.
• Discontinuing the drugs when symptoms have remitted may result in relapse.
• Untreated depressive episode is typically 6 to 9 months.
• When depressed patients take drugs for 3 to 4 months and then stop because they are
feeling better, they are likely to relapse because the underlying depressive episode is
actually still present, and only its symptomatic expression has been suppressed
• Because depression is often a recurrent disorder, physicians have increasingly
recommended that patients continue for very long periods of time on the drugs (ideally at
the same dose) in order to prevent recurrence.
• Thus, these medications can often be effective in prevention, as well as treatment, for
patients subject to recurrent episodes
Lithium and Other Mood-
Stabilizing Drugs
• Lithium therapy as a mood stabiliser – bipolar disorder
• mood stabilizer is often used to describe lithium and related drugs because
• they have both antimanic and antidepressant effects—that is,
• they exert mood-stabilizing effects in either direction
• Lithium is not more effective than other antidepressant
• Other antidepressants – precipitate manic phase or rapid cycling
• Lithium not such risk
• Prevents cycling between episodes
• Lithium therapy is maintained over long time periods, even when not manic or
depressed, to prevent new episodes.
• Side effects: lethargy, cognitive slowing, weight gain, decreased motor coordination,
kidney malfunction and same permanent damage and gastrointestinal difficulties.
• Poor compliance in taking drugs – side effects and missing symptoms of mania
• Another category of drugs – Anticonvulsants
• To patients who don’t respond to lithium or those having
unacceptable side effects
• Combination of lithium and anticonvulsants
• High risk of attempted and completed suicides
• Antipsychotic Medication for those (unipolar and
bipolar) who show psychotic symptoms along with
antidepressants and mood stabilisers
Alternative Biological
Treatments

• Electroconvulsive Therapy (ECT)


• Transcranial Magnetic Stimulation (TMS)
• Deep Brain Stimulation
• Neurofeedback
• Bright Light Therapy
Electroconvulsive Therapy (ECT)
• Induce seizures under general anesthesia and with muscle relaxants.
• used with severely depressed patients (especially among the elderly)
• who may present an immediate and serious suicidal risk,
• including those with psychotic or melancholic features
• who cannot take antidepressant medications or who are otherwise resistant to medications
• Complete remission of symptoms occurs in about 6 to 12 treatments (on alternate
day).
• Severely depressed patients can be vastly better in 2 to 4 weeks
• Most common side effect - confusion
• Lasting adverse effects on cognition, such as amnesia and slowed response time
• Antidepressants and lithium maintain gains of ECT and prevent relapse
• Useful in treating manic episodes
Transcranial Magnetic
Stimulation (TMS)
• Noninvasive technique allowing focal stimulation of the brain in
patients who are awake
• Brief but intense pulsating magnetic fields that induce electrical
activity in certain parts of the cortex
• Mainly unipolar patients who are resistant to other treatments
• Painless procedure
• Thousands of stimulations in each treatment session
• Treatment usually occurs 5 days a week for 2 to 6 weeks.
• Cognitive performance and memory are not affected adversely
Deep Brain Stimulation
• Implanting an electrode in the
brain and then stimulating
that area with electric current
• Those who do not respond to
medication, psychotherapy
and ECT
• Potential for treatment of
unrelenting depression
Neurofeedback
• It provides an individual with feedback about a specific
brain activity regarding a related behavior.
• Desired brain activity is rewarded while the undesired brain
activity is inhibited.
• Electroencephalography (EEG) was used in neurofeedback.
• functional magnetic resonance imaging (fMRI)
• functional near-infrared spectroscopy (NRIS)
• Depression, attention-deficit hyperactivity disorder, learning
disorders, traumatic brain injury, migraine, epilepsy, and
general cognitive performance
Bright Light Therapy

• This was originally used in the treatment of seasonal


affective disorder, but it has now been shown to be
effective in nonseasonal depressions as well
Psychotherapy
Specialized forms of psychotherapy for depression, alone or in
combination with drugs, significantly decrease the likelihood of relapse
within a 2-year follow-up period
• Cognitive-Behavioural Therapy
• Mindfulness based cognitive therapy
• Behavioural Activation Treatment
• Interpersonal Therapy
• Family and Marital Therapy
• Relapse Prevention Strategies
Cognitive-Behavioural

Therapy
Developed by Beck and colleagues • Mindfulness based cognitive therapy –
• Focuses on here-and-now problems for highly recurrent depression
• Highly structured, systematic attempts
• Taught to evaluate systematically their dysfunctional beliefs and
• Logic – depressed mood activates negative
negative automatic thoughts. thinking in recurrence
• To identify and correct their biases or distortions in information • Change the way in which these people relate
processing and
to their thoughts, feelings, and bodily
• To uncover and challenge their underlying depressogenic assumptions
and beliefs. sensations.
• Taught to treat their beliefs as hypotheses that can be tested • Group treatment involves training in
through the use of behavioral experiments. mindfulness meditation techniques aimed
• Brief form of treatment (usually 10 to 20 sessions) at developing patients’ awareness of their
• Depression with melancholic features unwanted thoughts, feelings, and sensations
• Highly effective – trained therapist so that they no longer automatically try to
• Preventing relapse and recurrence, similar to that obtained by
avoid them but rather learn to accept them for
staying on medication what they are—simply thoughts occurring in

the moment rather than a reflection of reality.
Medications target the limbic system, cognitive therapy may
have greater effects on cortical functions. • Useful in bipolar between episodes
• CBT and medications are equally effective in the treatment of
severe depression • Modified CBT with medication effective in
bipolar
Behavioural Activation
Treatment

• Focuses intensively on getting patients to become more active and engaged with their
environment and with their interpersonal relationships.
• Scheduling daily activities and rating pleasure and mastery while engaging in them,
exploring alternative behaviors to reach goals, and role-playing to address specific
deficits.
• Does not focus on implementing cognitive changes directly but rather on changing
behavior.
• To increase levels of positive reinforcement and to reduce avoidance and withdrawal
• Easier to train therapists to administer behavioral activation treatment than cognitive
therapy
Interpersonal Therapy
• Focuses on current relationship issues, trying to help the person understand and change
maladaptive interaction patterns
• As effective as medications or cognitive-behavioral treatment
• Useful in long-term follow-up for individuals with severe recurrent unipolar depression
• IPT and medication – lower recurrence rates

• Interpersonal and social rhythm therapy


• In bipolar - focus on stabilizing daily social rhythms
• Destabilized – precipitate bipolar disorder
• Taught to recognize the effect of interpersonal events on their social and circadian rhythms and to
regularize these rhythms.
• Along with medication
Family and Marital Therapy

• Stressor – unfavourable life situation


• Relapse – certain negative aspects of family
• Behaviour by a spouse can be interpreted by a former patient as criticism – relapse
• For ex, for bipolar disorder, some types of family interventions directed at
reducing the level of expressed emotion or hostility, and
• at increasing the information available to the family about how to cope with the disorder,
• have been found to be very useful in preventing relapse in these situations
• Marital therapy is given to unipolar patients with marital discord
• Increases marital satisfaction
Relapse Prevention Strategies
• A three-column relapse checklist during therapy sessions
along with homework for the patient.
• collaboratively filled with significant persons
• To describe all the changes in the patient’s sleep patterns, appetite,
interests, thought process, appearance, and so on.
• Discussing how the patient can cope with a relapse of the
manic or depressive episode.
• Identifying the first, middle, and late signs of a potential manic or
depressive relapse.
Conclusions
• Even without formal therapy, the great majority of patients with mania
and depression recover from a given episode in less than a year.
• With the modern methods of treatment discussed here, the general
outlook for a given episode if treatment is obtained has become
increasingly favorable for many, but by no means all, diagnosed
individuals.
• However, at least half never receive even minimally adequate treatment.
• Although relapses and recurrences often occur, these can now often be
prevented or at least reduced in frequency by maintenance therapy—
• through continuation of medication and
• follow-up therapy sessions at regular intervals.
• At the same time, the mortality rate for individuals
with depression is significantly higher than that for the
general population, partly because of the higher
incidence of suicide but also because there is an
excess of deaths due to natural causes, including
coronary heart disease.
• Patients with mania also have a high risk of death from
accidents (often with alcohol as a contributing factor),
neglect of proper health precautions, or physical
exhaustion.
• Thus, the need for still-more-effective treatment
methods, both immediate and long term, clearly
remains.
• Also, a great need remains to study the factors that put
people at risk for depressive disorders and to apply
relevant findings to early intervention and prevention.

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