Mood Disorders

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• Mood Disorders

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Mood Disorders

• Two key emotions on a continuum
• Depression
• Low, sad state in which life seems dark and
  overwhelming
• Mania
• State of breathless euphoria and frenzied energy

Depression
Mania
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Mood Disorders

• Most people with a mood disorder experience only
  depression
• This pattern is called unipolar depression
• Person has no history of mania
• Mood returns to normal when depression lifts
• Some people experience periods of depression that
  alternate with periods of mania
• This pattern is called bipolar disorder

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Mood Disorders

• These disorders have always captured peoples
  interest
• Millions of people have mood disorders
• Economic costs of mood disorders amount to more
  than 40 billion each year

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Unipolar Depression

• The term depression is often used to describe
  general sadness or unhappiness
• This usage confuses a normal mood swing with a
  clinical syndrome
• Clinical depression can bring severe and
  long-lasting psychological pain that may
  intensify over time

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How Common Is Unipolar Depression?

• 5 to 10 of the U.S. population experiences
  severe unipolar depression each year
• An additional 3 to 5 experience mild depression
• 17 of the world population experiences unipolar
  depression at some time in their lives
• Rates have been steadily increasing since 1915

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How Common Is Unipolar Depression?

• In almost all countries, women are twice as
  likely as men to experience severe unipolar
  depression
• Lifetime prevalence 26 of women vs. 12 of men
• These rates hold true across socioeconomic
  classes and ethnic groups
• 50 recover within six weeks, some without
  treatment
• Most will experience another episode at some point

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What Are the Symptoms of Depression?

• Symptoms may differ dramatically from person to
  person
• Five main areas of functioning may be affected
• Emotional symptoms
• feeling miserable, empty, humiliated
• Motivational symptoms
• lack drive, initiative, spontaneity
• 6 to 15 of those with severe depression commit
  suicide

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What Are the Symptoms of Unipolar Depression?

• Five main areas of functioning may be affected
• Behavioral symptoms
• less active, less productive
• Cognitive symptoms
• hold negative opinion of themselves
• blame themselves for unfortunate events
• Physical symptoms
• headaches, dizzy spells, general pain

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Diagnosing Unipolar Depression

• Criteria 1 Major depressive episode
• Marked by five or more symptoms lasting two or
  more weeks
• In extreme cases, symptoms are psychotic,
  including
• Hallucinations
• Delusions
• Criteria 2 No history of mania

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Diagnosing Unipolar Depression

• Two diagnoses to consider
• Major depressive disorder
• Criteria 1 and 2 are met
• Dysthymic disorder
• Symptoms are mild but chronic
• Experience longer-lasting but less disabling
  depression
• Consistent symptoms for at least two years
• When dysthymic disorder leads to major depressive
  disorder, the sequence is called double
  depression

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What Causes Unipolar Depression?The Biological
View

• Biochemical factors
• NTs serotonin and norepinephrine
• In the 1950s, medications for high blood pressure
  were found to increase depression
• Some lowered serotonin, others lowered
  norepinephrine
• Led to discovery of effective antidepressant
  medications
• It is likely not just one NT or the other a
  complex interaction is at work

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What Causes Unipolar Depression?The Biological
View

• Biochemical factors
• Endocrine system hormone release
• People with depression have been found to have
  abnormal levels of cortisol
• Released by the adrenal glands during times of
  stress
• People with depression have been found to have
  abnormal melatonin secretion
• Dracula hormone

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Cognitive Deficits in Depression

• Deficits in explicit verbal and visual memory,
  but not implicit memory
• Could be related to hippocampal volume
• Impairment in executive tasks
• Verbal fluency
• Set shifting
• Motor speed

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Cognitive Deficits in Depression

• It may be that depressed patients have more
  difficulty with effortful as compared to
  automatic tasks
• Motivational factors, particularly lack of reward
  sensitivity, may play a role
• Some cognitive deficits improve when there is
  inter-episode recovery, but there are still some
  cognitive scars (executive functioning, some
  types of memory)

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Cognitive Deficits in Depression- Limitations

• Localising neuropsychological tests may
  actually involve a number of brain regions
• Medication history
• Hx of symptoms

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Endophenotypes

• Children with a first-degree relative with mood
  disorder
• Verbal learning and suspectibility to
  interference
• Contradictory
• EF demands
• Social reasoning?
• Interaction with other biological factors (e.g.,
  thyroid dysfunction)

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Tissue volume loss

• Hippocampus results are contradictory
• Age
• Medication history
• Number of episodes
• Genetic factors
• Levels of circulating cortisol

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Tissue volume loss

• Orbitofrontal cortex and amygdala
• very preliminary
• affective processing
• Dorsolateral prefrontal cortex
• also preliminary
• cognitive processing
• Drug effects
• Cortisol

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Mayberg model of depression
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Goldapple et al. (2004)

• 2 groups 18 unmedicated, unipolar depressed
  outpatients and 13 patientstreated with drug
  (anti-depressant SSRI)
• CBT
• Drug
• Both approaches equally effective 50 percent
  success rate

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Goldapple et al. (2004)

• Cognitive behavior therapy is thought of as a
  top-down approach because it focuseson using
  thinking functions to modulateabnormal mood
  states, modify attentionand memory functions,
  change affective bias,and correct maladaptive
  informationprocessing

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Goldapple et al. (2004)

• CBT successful treatment increases incognitive
  processing regions (e.g.,hippocampus) and
  decreases in emotionalprocessing areas (e.g.,
  ventral medial cortex)

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Goldapple et al. (2004)

• Drug therapy is seen as a bottom-upapproach
  because it first changes thechemistry in the
  brainstem, limbic, and subcortical sites system.
• It then produces secondary cortical changeswith
  chronic treatment, altering more basicemotional
  and circadian behaviors andeventually causing
  upstream changes in depressive thinking.

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Goldapple et al. (2004)

• With drug therapy, metabolism (blood flow)
  decreases in the limbic area and increases in the
  cortical area.
• With CBT, limbic increases (in the hippocampus,
  dorsal mid cingulate) and cortical decreases (in
  the dorsolateral, ventrolateral, and medial
  orbital frontal inferior temporal and parietal).

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Goldapple et al. (2004)

• As CBT patients learn to turn off the thinking
  paradigm that leads them to dwell on negative
  thoughts and attitudes, activity in certain areas
  in the cortical (thinking, attention) region are
  decreasing as well.
• Drug leads to increases in cognitive oversight
  and decreases in ruminative, negative moodstates

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Goldapple et al. (2004)

• 2 types of depressed patients
• Differ at baseline

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• Lobotomys back!

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Anterior cingulotomy

• Advances in neurosurgical equipment
  andtechniques allow for new approaches
  totreating psychiatric problems
• Researchers have demonstrated that psychosurgery
  has helped a considerablenumber of
  treatment-resistant patients (lown)

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Counterpoint

• Withholding psychosurgery becomes ethically
  questionable for severely ill, treatment
  resistant patients
• A theoretical justification is not required
  forthe ethical use of psychosurgery, only
  adequate demonstrations of safety and efficacy
  (effectiveness) ???

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Bipolar Disorders

• People with a bipolar disorder experience both
  the lows of depression and the highs of mania
• They describe their life as an emotional roller
  coaster

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What Are the Symptoms of Mania?

• Unlike those experiencing depression, people in a
  state of mania typically experience dramatic and
  inappropriate rises in mood
• Five main areas of functioning may be affected
• Emotional symptoms
• active, powerful emotions in search of outlet
• Motivational symptoms
• need for constant excitement, involvement,
  companionship

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What Are the Symptoms of Mania?

• Five main areas of functioning may be affected
• Behavioral symptoms
• very active move quickly talk loudly or
  rapidly
• Key word flamboyance!
• Cognitive symptoms
• show poor judgement or planning
• Especially prone to poor (or no) planning
• Physical symptoms
• high energy level often in the presence of
  little or no rest

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Diagnosing Bipolar Disorders

• Criteria 1 Manic episode
• Three or more symptoms of mania lasting one week
  or more
• In extreme cases, symptoms are psychotic
• Criteria 2 History of mania
• If currently experiencing hypomania or depression

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Diagnosing Bipolar Disorders

• Two kinds of bipolar disorder
• Bipolar I disorder
• Full manic and major depressive episodes
• Most sufferers experience an alternation of
  episodes
• Some experience mixed episodes
• Bipolar II disorder
• Hypomanic episodes and major depressive episodes

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Diagnosing Bipolar Disorders

• Without treatment, the mood episodes tend to
  recur for people with either type of bipolar
  disorder
• If people experience four or more episodes within
  a one-year period, their disorder is further
  classified as rapid cycling
• If their episodes vary with the seasons, their
  disorder is further classified as seasonal

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Diagnosing Bipolar Disorders

• Between 1 and 1.5 of adults in the world suffer
  from a bipolar disorder at any given time
• The disorders are equally common in women and men
• Women may experience more depressive and fewer
  manic episodes than men
• Rapid cycling is more common in women

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What Causes Bipolar Disorders?

• Neurotransmitters (NTs)
• After finding a relationship between low
  norepinephrine and unipolar depression, early
  researchers expected to find a link between high
  norepinephrine and mania
• This theory is supported by some research
  studies bipolar disorders may be related to
  overactivity of norepinephrine

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What Causes Bipolar Disorders?

• Neurotransmitters (NTs)
• Because serotonin activity often parallels
  norepinephrine activity in unipolar depression,
  theorists expected that mania would also be
  related to high serotonin activity
• While no relationship with HIGH serotonin has
  been found, bipolar disorder may be linked to LOW
  serotonin activity, which seems contradictory

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What Causes Bipolar Disorders?

• Neurotransmitters (NTs)
• This apparent contradiction is addressed by the
  permissive theory about mood disorders
• Low serotonin may open the door to a mood
  disorder and permit norepinephrine activity to
  define the particular form the disorder will
  take
• Low serotonin Low norepinephrine Depression
• Low serotonin High norepinephrine Mania

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What Causes Bipolar Disorders?

• Ion activity
• Ions, which are needed to send incoming messages
  to nerve endings, may be improperly transported
  through the cells
• This improper transport may cause neurons to fire
  too easily (mania) or to resist firing
  (depression)
• There is some research support for this theory

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Hippocampal volume INCREASES

• We have reported increases in hippocampal volume
  in BD patients both cross-sectionallyand
  prospectively
• Lithium
• Other antipsychotics
• No drug
• Control

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Dx PTSD

• A. The person has been exposed to a traumatic
  event in which both of the following have been
  present 
• (1) the person experienced, witnessed, or was
  confronted with an event or events that involved
  actual or threatened death or serious injury, or
  a threat to the physical integrity of self or
  others

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Dx PTSD

• A. The person has been exposed to a traumatic
  event in which both of the following have been
  present 
• (2) the person's response involved intense fear,
  helplessness, or horror. Note In children,
  this may be expressed instead by disorganized or
  agitated behavior.

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Dx PTSD

• B. The traumatic event is persistently
  reexperienced in one (or more) of the following
  ways 
• (1) recurrent and intrusive distressing
  recollections of the event, including images,
  thoughts, or perceptions. Note In young
  children, repetitive play may occur in which
  themes or aspects of the trauma are expressed.

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Dx PTSD

• B. The traumatic event is persistently
  reexperienced in one (or more) of the following
  ways 
• (2) recurrent distressing dreams of the event.
  Note In children, there may be frightening
  dreams without recognizable content.

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Dx PTSD

• B. The traumatic event is persistently
  reexperienced in one (or more) of the following
  ways 
• (3) acting or feeling as if the traumatic event
  were recurring (includes a sense of reliving the
  experience, illusions, hallucinations, and
  dissociative flashback episodes, including those
  that occur upon awakening or when intoxicated).
  Note In young children, trauma-specific
  reenactment may occur.

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Dx PTSD

• B. The traumatic event is persistently
  reexperienced in one (or more) of the following
  ways 
• (4) intense psychological distress at exposure to
  internal or external cues that symbolize or
  resemble an aspect of the traumatic event.
• (5) physiological reactivity on exposure to
  internal or external cues that symbolize or
  resemble an aspect of the traumatic event.

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Dx PTSD

• C. Persistent avoidance of stimuli associated
  with the trauma and numbing of general
  responsiveness (not present before the trauma),
  as indicated by three (or more) of the
  following 
• (1) efforts to avoid thoughts, feelings, or
  conversations associated with the trauma 
• (2) efforts to avoid activities, places, or
  people that arouse recollections of the trauma 
• (3) inability to recall an important aspect of
  the trauma 

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Dx PTSD

• C. Persistent avoidance of stimuli associated
  with the trauma and numbing of general
  responsiveness (not present before the trauma),
  as indicated by three (or more) of the
  following 
• (4) markedly diminished interest or participation
  in significant activities 
• (5) feeling of detachment or estrangement from
  others 

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Dx PTSD

• C. Persistent avoidance of stimuli associated
  with the trauma and numbing of general
  responsiveness (not present before the trauma),
  as indicated by three (or more) of the
  following 
• (6) restricted range of affect (e.g., unable to
  have loving feelings) 
• (7) sense of a foreshortened future (e.g., does
  not expect to have a career, marriage, children,
  or a normal life span)

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Dx PTSD

• D. Persistent symptoms of increased arousal (not
  present before the trauma), as indicated by two
  (or more) of the following 
• (1) difficulty falling or staying asleep 
• (2) irritability or outbursts of anger 
• (3) difficulty concentrating 
• (4) hypervigilance 
• (5) exaggerated startle response

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Dx PTSD

• E. Duration of the disturbance (symptoms in
  Criteria B, C, and D) is more than one month.
• F. The disturbance causes clinically significant
  distress or impairment in social, occupational,
  or other important areas of functioning.

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Dx PTSD

• Specify if 
• Acute if duration of symptoms is less than 3
  months 
• Chronic if duration of symptoms is 3 months or
  more
• Specify if 
• With Delayed Onset if onset of symptoms is at
  least 6 months after the stressor

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Post-Traumatic Stress Disorder

• Survivor guilt
• Phobic avoidance interpersonal relationships
  lead to marital conflict, divorce, or loss of
  job.

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Post-Traumatic Stress Disorder

• The following associated constellation of
  symptoms may occur and are more commonly seen
  in association with an interpersonal stressor
• feelings of ineffectiveness, shame, despair,
  or hopelessness feeling permanently damaged a
  loss of previously sustained beliefs, hostility
  social withdrawal feeling constantly
  threatened impaired relationships with others
  or a change of the individual's previous
  personality characteristics.

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Hyper and hypoactivation

• Cognitive processing regions
• Dorsolateral PFC
• Hippocampus
• Emotional processing regions
• Oribitofrontal
• Medial frontal

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Hippocampal volume loss

• Appears consistent across number of studies
• Drug effects
• Elevated cortisol over time
• Twin study (Gilbertson et al., 2002)

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Air Transat Flight 236
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September 11th, 2001
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Emotion and memory

• Emotion enhances memory and attention (e.g., word
  lists, images flashbulb memories)

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Emotion and memory

• Alters the neural activity involved in
  recollection (including AM)

Svoboda, McKinnon, Levine, submitted
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Traumatic AM

• Traumatic AM seldom studied for real-life,
  personal events
• Laboratory studies (Loftus, 1975 Christianson,
  1992)
• weapons effect
• Flashbulb memory (witnessed events Brown
  Kulik, 1977 Weaver, 1993)

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Traumatic AM

• Personal trauma
• Alterations in memory following trauma (in PTSD)
• Overgeneralized memory for events not related to
  trauma
• similar to other disorders that involve
  alterations in frontal function (depression,
  schizophrenia, borderline personalitydisorder)

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Traumatic AM

• Vulnerable to the encoding of false memories
  source monitoringdeficit (Clancy, Schacter,
  McNally, Pitman, 2000)

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Traumatic AM

• Few studies have examined memoryfor trauma
  itself
• traumatic memories characterized asimpoverished
  and fragmented (van der Kolk Fisher, 1995
  Tromp et al., 1995)
• early childhood abuse as high as 60 (Terr,
  1991) period of childhood amnesia

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Traumatic AM

• Few studies have examined memoryfor trauma
  itself
• Other studies high rate of memory accuracy,
  particularly for non-PTSD (Yuille, 1986
  Schelach Nachson, 2001)
• differ widely in arousal, retention interval,
  event characteristics
• unclear whether survey episodic or semantic AM

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Traumatic AM

• Apparent paradox in DSM-IV-TR where PTSD is
  thought to involve an
• inability to recall an important aspect of the
  trauma
• Avoidance symptoms (suggests voluntary control?)
• Contrasts with flashbacks (involuntary) also
  described

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Our study

• AT Flight 236 passengers
• PTSD versus non-PTSD
• Matched controls

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Our study

• Autobiographical memory interview
• Episodic and semantic recall
• Qualitative (e.g., perceptual versus emotional)
• Difficult-to-retrieve memories (Steinvorth,
  Levine Corkin, 2005)

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Method

• 3 events
• AT (Controls highly negative memory)
• September 11th, 2001 (witnessed flashbulb)
• Everyday event from same time period

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(No Transcript)
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Hypotheses

• AT passengers will show enhanced recollection of
  the AT disaster relative to other emotional and
  non-emotional events.
• Relative to passengers without PTSD, passengers
  with PTSD willshow both enhanced recollection of
  the AT disaster and impoverished recollection of
  non-emotional autobiographical events.
• These effects will be specific to episodic
  (rather than semantic) information.

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Results
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Results