Abnormal Psychology - Final Flashcards
What is a diagnosis
assigning a patient’s symptoms to a specific classification
What is a clinical assessment
obtaining relevant information and making a judgment based on it
Assessment is collecting relevant information in an effort to reach a conclusion
used to determine how & why a person is behaving abnormally and how that person may be helped
Focus is idiographic (i.e., on an individual person)
psychodynamics: looking at symbols they might be using
behavioral: what behaviors do you exhibit
Also may be used to evaluate treatment progress
What is prevalence
number of people who have a disorder in a given period of time (e.g., life-time prevalence)
What is incidence
total number of new cases identified in a given period of time (e.g. 12-month)
Briefly describe what is the DSM-5
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and Fourth Edition, Text Revision (DSM-IV-TR)
Describes characteristics of many psychological disorders
Identifies criteria, kinds, number, and duration of relevant symptoms
Categorical system; Used in North America
Briefly describe the ICD-11
International Classification of Diseases, 10th Edition (ICD-10) & 11th Edition (ICD-11)
Includes both general medical and psychological disorders
Used in other parts of the world
Name 3 categories of the ICD-10 from the chapter 6: Mental, behavioural and neurodevelopmental disorders
Neurodevelopmental disorders
Schizophrenia or other primary psychotic disorders
Catatonia
Mood disorders
Anxiety or fear-related disorders
Obsessive-compulsive or related disorders
Disorders specifically associated with stress
Dissociative disorders
Feeding or eating disorders
Elimination disorders
Disorders of bodily distress or bodily experience
Disorders due to substance use or addictive behaviours
Impulse control disorders
Personality disorders and related traits
Paraphilic disorders
Neurocognitive disorders
Name 6 uses for the DSM
- common language for clinicians
- tool for researchers
- clinical/research interface
- information for educators and students
- coding system for statistical, insurance, and administrative purposes.
- important role in both civil and criminal legal proceedings
Name 4 downsides to using the DSM
- criteria are somewhat too detailed to be completely convenient to clinicians
- not quite detailed enough for the taste of researchers
- too dull for teachers and students
- not nearly precise enough for lawyers
What was Emil Kraepelin’s contribution (4)
- Created a classification system to establish the biological nature of mental illnesses
- Noticed clustering of symptoms (syndrome) which were presumed to have an underlying physical cause,
each mental illness is seen as distinct, with own genesis, symptoms, course, and outcome - Proposed two major groups of severe mental diseases (affective vs non-affective)
a. Dementia praecox (early term for schizophrenia)
chemical imbalance as the cause of schizophrenia
b. Manic-depressive psychosis (now called bipolar disorder)
irregularity in metabolism as the cause of manic-depressive psychosis
4.proposed that they had different biological underlying causes
Kraepelin’s early classification scheme became the basis for the present diagnostic categories
Explain the development of the DSM
1952: DSM psychodynamically oriented
“neurosis reaction,” “personality disturbance”
130 pages, 106 disorders
1968: DSM II: still psychodynamically oriented
broad descriptions, symptoms not specified in detail
“neurosis,” “psychosis”
134 pages, 182 disorders
In 1980, the APA published an extensively revised diagnostic manual (DSM-III); and then revised it further in 1987 (DSM-III-R) Focused on reliability and validity Did not rest on psychodynamic theory Focused on observations, not inferences Listed explicit criteria for each disorder and used research to develop the criteria Introduced the multiaxial system 494 pages, 265 disorders (DSM–III) 567 pages, 292 disorders (DSM-IIIR)
DSM-IV was published in 1994 and the APA subsequently completed a “text revision” (DSM-IV-TR; APA, 2000)
Overall DSM-IV
Included more current information about each disorder
Prevalence, course, gender and cultural factors
Comorbidity – the presence of more than one disorder at a time in a given patient
DSM-V - published in May 2013
How did both the ICD and DSM started to introduce mental illness (3)
1939 - World Health Organization (WHO) added mental disorders to the International List of Causes of Death
1948 - the list expanded to become part of the International Statistical Classification of Diseases, Injuries, and Causes of Death (ICD-6)
1952 - American Psychiatric Association (APA) published its own Diagnostic and Statistical Manual (DSM) in 1952
Name 5 major changes from the DSM-IV to the DSM-5
- Autism Spectrum Disorder (ASD): Asperger’s now eliminated, part of ASD
- Obsessive-Compulsive and Related Disorders: OCD removed from the anxiety disorders and moved under this new heading
- Trauma and Stressor-Related Disorders: post traumatic stress disorder (PTSD) is now in this separate category
- Substance-Related and Addictive Disorders: now include non-substance-related addiction, i.e. gambling
- Subtypes of schizophrenia: (paranoid, disorganized, catatonic, and undifferentiated) have been eliminated
What is the multi-axial system
people would be rated on every axis (axis 1 to 5)
all of the psychopathologies except personality disorders
axis 1: clinical disorders (depression, bipolar, schizophrenia, etc.)
axis 2: personality disorders (borderline, antisocial, etc.)
axis 3: general medical conditions (infectious disease, etc.)
axis 4: psychosocial and environmental problems (jobs less, etc.)
axis 5: global assessment of functioning (0-100)
Eliminated from the DSM 5
Describe the 3 main findings in the Frances & Widiger (2012) article, view on mental disorders
there are currently at least 3 ways that we (as researchers, practitioners, educators, students, general population and people with actual diagnosis) understand mental disorders and DSM system
- Mental disorders are real things
mental disorders are real things existing ‘out there’ that will soon reveal their secrets through scientific study. This has been the predominant view among biological psychiatrists, but it is now recognized to be a misleading and reductionist simplification - Mental disorders are heuristic constructs
mental disorders are no more than useful heuristic constructs. This is now the consensus of most serious students of mental illness, including some of the most fervent biological psychiatrists - Mental disorders are social constructs
mental disorders will never be fully understood; they are social constructs - subject to arbitrariness an misuse
Name 5 professional and social contextual forces that impact diagnostic of mental disorders
- starting with DSM-III psychiatric diagnosis became accessible to the general public
- it is fairly easy to meet criteria for one or another DSM diagnosis
- the role of pharmaceutical industry
- the role of media
- we live in a society that is perfectionistic (as individualistic)
Name 4 recent epidemics (over diagnosis)
- autism
- attention deficit
- childhood bipolar disorder
- paraphilia not otherwise specified
Name 3 criticisms of using a classification system
- DSM categories refer to hypothetical constructs that may or may not exist in reality
- psychiatric diagnoses are different from most medical diagnoses where the basic cause is frequently known an the presence of the disease can usually be objectively determined (e.g. blood or urine test)
- psychiatric diagnosis appear to be influenced by fads that provoke overdiagnosis, also referred to as epidemics
Name 3 DSM-5 specific criticisms
- lowering age requirements for some categories promote what is already an alarming overuse of pharmacotherapy in children - sometimes causing serious side effects: obesity, diabetes, cardiovascular complications, etc.
- lowered thresholds for existing categories and the invention of new disorders increases the already high rates of ADHD, PTSD, GAD, substance dependence
- the overall result - an unintended medicalization of normality with consequent overtreatment, stima, and misallocation of scarce mental health resources
What is the difference between a discrete entity and a continuum
the DSM represents a categorical classification, a yes-no approach
continuity argument - abnormal and normal behaviors differ only in intensity or degree, not in kind; therefore, discrete diagnostic categories foster a false impression of discontinuity
in dimensional classification, the entities or objects being classified must be ranked on a quantitative dimension (e.g. a 1-to-10 scale of anxiety)
Describe interviews as psychological assessments
Psychological assessment techniques are designed to determine cognitive, emotional, personality, and behavioral factors in psychopathological functioning
many of the assessment techniques stem from the paradigms we discussed earlier during the course
- Clinical Interview
Initial assessment
History of clients and their current problem(s)
Allows for direct observation of a client
Great skills required to establish rapport and trust
highly important so they don’t feel judged - Structured and Semi-structured Interviews
SCID (Structured Clinical Interview for DSM)
most widely used (clinician, research more detailed, forensic)
Diagnosis of psychopathology
Allow for direct observation of a client
Name 3 psychological test as psychological assessment
3 basic types of tests:
self-report personality inventories
projective personality tests
tests of intelligence
Describe the projective personality tests
a set of standard stimuli (inkblots or drawings) ambiguous enough to allow variation in responses
assumption is that because the stimulus materials are unstructured, the client’s responses will be determined primarily by unconscious processes and will reveal his or her true attitudes, motivations, and modes of behavior
Name 5 types of projective personality tests
- Rorschach Inkblot Test (traditional inkblot)
- Thematic Apperception Test (TAT)
Sees a scene and must attribute a scenario and thoughts to the scene - Roberts Apperception Test for Children
- Sentence completion tests
“I wish …___________________________”
“My father… ________________________” - Drawings
“Draw a person”
“Draw another person of the opposite sex”
Name 4 Intelligence tests
- Wechsler Adult Intelligence Scale (WAIS)
- Wechsler Intelligence Scale for Children (WISC)
- Stanford-Binet
- emotional intelligence (EQ) reflected in such abilities as delaying gratification and being sensitive to the needs of others, may be as important to future success as the strictly intellectual achievements measured by traditional IQ tests. Moreover, high levels of emotional intelligence are associated with greater levels of subjective well-being and reduced proneness to depression
Name 2 types of behavioural and cognitive assessment and one drawback
Direct Observation of Behaviour
observe if the non-verbal matches the verbal (e.g. talking about horrific things with a smile)
Self-Observation (self- monitoring) – also referred to as ecological momentary assessment (EMA) - involves the collection of data in real time as opposed to the more usual methods of having people reflect back over some time period and report on recently experienced thoughts, moods, or stressors
phone app, mood trackers
However – reactivity
people know they are observed
Name 2 types of neuroimaging methods reflecting direct neuronal activity
EEG – electroencephalography
MEG – magnetoencephalography
Name 2 types of neuroimaging methods reflecting tomographic information
PET – positron emission tomography
SPET – single photon emission tomography
Name 4 types of magnetic resonance imaging (MRI) methods:
MRI – structural
fMRI - functional
DTI – diffusion tensor imaging
MRS – magnetic resonance spectroscopy
Why use EEG or MEG in abnormal psychology
we cannot diagnose anybody with scans for psychopathologies resting state/spontaneous activity sleep pattern event-related potential (ERPs) biofeedback
Why use PET scans in abnormal psychology
Resting state metabolism (FDG PET)
cannot look at resting state in fMRI
we can label glucose
Cerebral blood flow (O-15 PET)
we can label oxygen
Neurotransmission (assessing specific receptor occupancy)
look how much antipsychotic (D2 antagonist) and if we could see the receptor occupancy we could limit side effects by finding the optimal dosing, however that is really expensive
Why use MRI in abnormal psychology
observe the difference in the brain structures of people with mental disorder vs healthy
What can you measure in the autonomic nervous system to try to understand the nature of emotions
Activities of the autonomic nervous system are frequently assessed by electrical and chemical measurements in an attempt to understand the nature of emotion.
Heart rate measured with electrocardiogram
Skin conductance measured with electrodermal responding
Brain activity measured by electroencephalogram (EEG)
How do you do a neurochemical assessment (3)
- Analyzing the metabolites of various neurotransmitters that have been broken down by enzymes in a urine, blood, and cerebrospinal fluid samples
- Assessing density of neurotransmitter receptors post mortem
- Biological assessments cannot be used to diagnose psychopathology but can play a role in its accuracy (e.g., neurodegenerative dementia vs. vascular dementia) and in exclusion of any major brain anomalies (e.g., tumor)
Why do a neuropsychological assessment (5)
Some tests are believed to detect effects of brain damage that are not (yet) detectable by neurological examination
selected goals of neuropsychological testing
- measure the behavioral correlates of brain function
- establish possible localization, lateralization, and etiology of a brain lesion
- describe neuropsychological strengths, weaknesses, and strategy for problem solving
- assess patient’s feelings about his or her syndrome
- provide treatment recommendations (i.e., to client, family, school)
What distinguishes fear from anxiety?
Fear is a state of immediate alarm in response to a serious, known threat to one’s well-being
Anxiety is a state of alarm in response to a vague sense of being in danger
Both have the same physiological features – increase in respiration, perspiration, muscle tension, etc.
The implicated neural circuitry might differ slightly
Which neural circuit in involved in fear response
Fear response: central nucleus of the amygdala plays a role in response to sudden, aversive events
Which structure of the brain is involved in both anxiety and fear
Both fear and anxiety are associated with the amygdala, but there are some differences in the circuitry
Which part of the brain is involved in anxiety
amygdala and prefrontal cortex connection
bed nucleus of the stria terminalis (BNST) initiates emotional response when stimuli are less precise predictors of potential danger. This produces a state of sustained preparedness for an unclear danger and prolonged anticipation of unpleasantness.
amygdala aids in formation of emotional memories and conditioned fear or conditioned emotional response, which establishes quickly and is long-lasting
amygdala also contributes to memory consolidation through its connections with the hippocampus
Anxiety disorders are often considered to arise from an imbalance between emotion generating centers and higher cortical control
Which main hormone is involved in anxiety
Corticotropin-releasing factor (CRF) is released from the hypothalamus in response to stress/fear/anxiety
Acts on releasing cortisol, adrenaline and noradrenaline. Overall overactivation of the sympathetic nervous system
How is norepinephrine involved in anxiety
Norepinephrine is involved, important in the formation of emotional memories
NE antagonists reduces anxiety, impair the formation of emotional memories, can block traumatic memories, helps PTSD
NE agonist can lead to panic attacks
How is GABA involved in anxiety
inhibitory neurotransmitter
Benzodiazepines (BDZ) & barbiturates cause sedation and reduced anxiety by binding to modulatory sites of GABA
gaba agonist
GABA antagonists can produce extreme anxiety and panic
GABA & neurosteroids
Neuroactive steroids such as progesterone (which fluctuates across the menstrual cycle) and testosterone (higher levels in men) provide an additional modulatory role in anxiety (they bind to a separate site on GABAA)
Neurosteroids levels tend to be low in people with generalized anxiety disorder and social phobia
Name 6 Major Anxiety Disorders in DSM-IV and which ones were excluded in DSM-5
- Phobia
- Panic Disorder
- Generalized Anxiety Disorder
- Obsessive-Compulsive Disorder
- Post-Traumatic Stress Disorder
- . Acute Stress Disorder
DSM 5 excludes OCD (new section) and PTSD (to Trauma and stress-related disorder)
Name 2 inclusions in the DSM-5 of anxiety disorders
Separation Anxiety Disorder
classified previously in the section “Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence”
diagnostic criteria no longer specify that age at onset must be before 18 years, but the duration criteria of 6 months added
Selective Mutism classified previously in the section “Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence” classified as an anxiety disorder because a majority of children with selective mutism are anxious diagnostic criteria largely unchanged from DSM-IV children where nothing wrong with language development and communication skills, in specific context they stop talking (e.g. does not talk in school, but they do in their families) fairly involuntary (not just a choice)
Describe the prevalence and common demographics for anxiety disorders
the most common psychological disorders
early age of onset, typically during childhood-adolescence
quite common among university students
more common in women than in men across all age groups
hormonal component, with depression pronounced during reproductive age, but not reproductive age correlation with anxiety
the highest one-year prevalence rates found in women 15 to 24 years of age
gender differences found in 15 countries around the world
What does the comorbidity among anxiety disorders mean
symptoms of the various anxiety disorders are not entirely disorder specific (e.g., perspiration, fast heart rate)
the etiological factors that give rise to various anxiety disorders are probably applicable to more than one disorder (e.g., related to childhood maltreatment and/or ANS dysregulation)
causes are similar but the expression may vary
Yet, theories of anxiety disorders focus on individual disorders; development of theories that take comorbidity into account is a challenge for the future
Describe the comorbidity within anxiety disorders & with other conditions
co-occurrence of the anxiety disorders (panic disorder, GAD, SAD)
is it 3 different issues, or the same one expressed in many ways
anxiety disorders are often comorbid with substance abuse, depression, PTSD, OCD
self medication with alcohol, alcohol binds on GABA receptors just like benzodiazepines
anxiety disorders are also independent risk factors for suicide attempts
Comorbidity of anxiety disorder is the strongest with which other disorder
is strongest with depressive disorders
anxiety and depression appear to be related to each other at both genotypic and phenotypic levels
e.g., behavioral genetic analysis of major depression, panic disorder, agoraphobia, and SAD showed that the disorders strongly co-aggregate within families
Describe the Tripartite Model of Anxiety and Depression
Anxiety: Physiological hyperarousal
Depression: Lack of enjoyment (low level of positive emotions)
Overlap of anxiety + depression: General distress (high level of negative emotions)
he model posits that anxiety and depression share a common component of negative affect/general distress; however, they can be differentiated by physiological hyper-arousal (hypothalamic-pituitary-adrenal axis) associated with anxiety and by low positive affect (anhedonia) associated with depression.
Which theories (2) are the most common with anxiety disorders
2 most common: cognitive & biological theories
a common theme across all anxiety disorders is that dysfunctional levels of anxiety reflect cognitive appraisal processes contributing to the perception of anxiety, as well as physiological factors that render particular people more vulnerable to anxiety
What are phobias
Psychopathologists define a phobia as a disrupting, fear-mediated avoidance that is out of proportion to the danger actually posed (according to DSM-5 it does not need to be recognized by the sufferer as excessive or unreasonable, but it was the case for DSM-IV)
The term “phobia” usually implies that the person suffers intense distress and social or occupational impairment because of the anxiety
Many specific fears do not cause enough hardship to compel an individual to seek treatment (e.g., an urban dweller with an intense fear of bears)
Psychologists tend to focus on different aspects of phobias according to the paradigm they have adopted
Contrast the psychoanalyst views with the behaviourist views on phobias
Psychoanalysts focus on the content of the phobia and see the phobic object as a symbol of an important unconscious fear (e.g., fear of the father transformed into fear of horses in the case of Little Hans)
Behaviorists, on the other hand, tend to ignore the content of the phobia and focus instead on its function (e.g., fear of horses and fear of heights are equivalent in the means by which they are acquired, in how they might be reduced, and so on)
How common are specific phobias, when does it start, which are most common
lifetime prevalence - almost 1 in 10!
mean age of onset - around 10 years old
mean duration - about 20 years
only 8% with a specific phobia received treatment
the most common specific phobia subtypes in order:
(1) animal phobias (including insects, snakes, birds)
(2) heights
(3) being in closed spaces
(4) flying
(5) thunderstorms
(6) blood
Name 2 culture specific phobias
Chinese Paleng - a fear of the cold (fear that loss of body heat may be life-threatening); presumably related to the Chinese philosophy of yin and yang
Japanese taijin kyofusho (TKS) - fear of other people - not a social phobia, but an extreme fear of embarrassing others. Apparently arises from elements of traditional Japanese culture, which encourages extreme concern for the feelings of others yet discourages direct communication of feelings (McNally, 1997)
Describe Social Anxiety Disorder (SAD)
social phobia = social anxiety disorder
Marked, disproportionate, and persistent fears about one or more social situations
May be narrow – talking, performing, eating, or writing in public
May be broad – general fear of functioning poorly in front of others
In both forms, people rate themselves as performing less competently than they actually do
can be extremely debilitating
What is the prevalence and demographic of SAD
onset typically in adolescence (around 13-15 yrs)
the lifetime prevalence about 6-7% in men and 8-9% in women
average duration of symptoms about 20 years
comes with age, we care less about making fools of ourselves as we age
prevalence of social phobia higher among single people, those who have not completed secondary education, had lower income or were unemployed
not the cause, but the results of SAD
What is the three-factor model of SAD
(1) social interaction fears
(2) observation fears: being observed is very uncomfortable
(3) public speaking fears
What is the SAD comorbidity
high comorbidity rate with other disorders, such as GAD, specific phobias, panic disorder, avoidant personality disorder, and mood disorders
high levels of comorbidity with heavy drinking and alcohol dependence, as well as marijuana- related problems
Describe the etiology of Phobias - behavioral perspective (conditioning), which criticisms
avoidance-conditioning
via classical conditioning, a person can learn to fear a neutral stimulus (the CS) if it is paired with an intrinsically painful or frightening event (the UCS).
the person can learn to reduce this conditioned fear by escaping from or avoiding the CS. This second kind of learning is assumed to be operant conditioning; the response is maintained by its reinforcing consequence of reducing fear.
starts as a trigger (classical) and is reinforced through avoidance (operant)
however, evidence demonstrates that only some (certainly not all) fears may be acquired in this particular way
Some people become intensely afraid of heights after a bad fall, etc.
However, many individuals with severe fears of snakes, germs, and airplanes tell clinicians that they have had no particularly unpleasant experiences with these objects or situations…
Describe the etiology of Phobias - behavioral perspective (modeling)
a person can learn fears through imitating the reactions of others (vicarious learning )
e.g., Bandura and Rosenthal (1966) - after the participants had watched the model “suffer” a number of times, they showed an increased frequency of emotional responses when the buzzer sounded
vicarious learning may also be accomplished through verbal instructions (e.g., the anxious-rearing model is based on the premise that anxiety disorders in children are due to constant parental warnings that increase anxiety in the child)
What is prepared learning the the context of phobias
prepared learning, biological predisposition to certain stimuli
people tend to fear only certain objects and events, such as spiders and heights, but not others, such as flowers
some fears may well reflect classical conditioning, but only to stimuli to which an organism is physiologically prepared to be sensitive
Describe the etiology of SAD - cognitive perspective
People with SAD are
- more concerned about evaluation (high degree of public self-consciousness)
- preoccupied with hiding imperfections and not making mistakes (perfectionistic standards for accepted social performances)
- tend to view themselves negatively even when they have actually performed well in a social interaction (an attentional bias to focus on negative social information and interpret ambiguous situations as negative)
Cognitive theorists contend that people with this disorder hold a group of social beliefs and expectations that consistently work against them
Give examples of a cognitive expectations of SAD
- unrealistically high social standards, thus must perform perfectly in social situations
- view themselves as unattractive social beings
- view themselves as socially unskilled and inadequate
- believe they are always in danger of behaving incompetently in social situations
- believe that inept behaviors in social situations will inevitable lead to terrible consequences
- believe that they have no control over feelings of anxiety that emerge during social situations
Name 3 types of phobias that have arise from social media
- FoMO (fear of missing out)
- nomophobia (no mobile phone phobia)
- online social anxiety
Describe the etiology of phobias - predisposing biological factors
biological malfunction (a diathesis) that somehow predisposes some people to develop a phobia following a particular stressful event
the prevalence of social and specific phobias is higher than average in first-degree relatives
However
learning cannot be ruled out
no specific genes have been found
Describe the etiology of phobias - psychoanalytic theories
According to Freud, phobias are a defense against the anxiety produced by repressed id impulses
This anxiety is displaced from the feared id impulse and moved to an object or situation that has some symbolic connection to it
By avoiding these symbolic (and now phobic) objects or situations the person is able to avoid dealing with repressed conflicts
As with most psychoanalytic theorizing, evidence is restricted to conclusions drawn from clinical case reports
Name 6 types of treatment with a behavioural approach to phobias
- Systematic desensitization - the first major behavioral treatment to be used widely and successfully in treating phobias
- exposure-based treatment outperformed both placebo conditions and other psychotherapeutic approaches
- virtual reality (in some studies as effective as real-life exposure) may be a nice alternative
- Modeling - fearful clients are exposed to filmed or live demonstrations of other people interacting fearlessly with the phobic object (e.g., touching spiders)
- Flooding - extreme discomfort is inevitable
- Operant techniques - real-life exposures to the phobic object are gradually achieved, and the client is rewarded for even minimal successes
Therapies for phobias – cognitive approaches
viewed with skepticism - if the person already acknowledges that the fear is of something harmless, what use can it be to alter the person’s thoughts about it?
for social phobias, cognitive methods—sometimes combined with social skills training—are more promising.
to more accurately appraise people’s reactions to them
to rely less on the approval of others for a sense of self-worth
Therapies for phobias - Biological approaches
GABA agonists - barbiturates - the first major category of drugs used to treat anxiety disorders, but highly addictive + great risk of a lethal overdose –replaced in the 1950s by benzodiazepines
monoamine oxidase (MAO) inhibitors show some effectiveness especially with social phobias, but can lead to weight gain, insomnia, sexual dysfunction, and hypertension
selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac) have also shown some promise in reducing social phobia
Problems – side effects + the client may find it difficult to discontinue their use, relapse being a common result
Therapies for phobias - Psychoanalytic approaches
Classical psychoanalytic treatments of phobias attempted to uncover the repressed conflicts believed to underlie the extreme fear and avoidance characteristic of these disorders
Contemporary ego analysts focus less on gaining historical insights and more on encouraging the client to confront the phobia. However, they do view the phobia as an outgrowth of an earlier problem
Describe Panic Attack
person suffers a sudden and often inexplicable attack of alarming symptoms (typically lasts for several minutes, rarely hours):
labored breathing, heart palpitations, chest pain, nausea, feelings of choking, dizziness, sweating, trembling
intense apprehension, terror, and feelings of impending doom
may also experience depersonalization and de-realization
Recurrent un-cued attacks and worry about having attacks in the future are required for the diagnosis of panic disorder.
Describe Panic Disorder
PD features:
Frequent, unexpected panic attacks
(Cued – associated with particular objects, situations, or sensations; present in phobias or PTSD)
Uncued – spontaneous, not associated with a particular object or situation
Can occur at anytime, even when sleeping (nocturnal panic attacks)
In DSM-IV diagnosed as with or without agoraphobia (in DSM-5 these are two distinct diagnoses)
What is the prevalence of panic disorders
Lifetime prevalence
2-3% for men; 5-6% for women
Low SES 50% more likely to develop them
Typically begins in adolescence
Onset associated with stressful life experience
> 80% of patients diagnosed as having an anxiety disorder also experience panic attacks
What is the prevalence of Panic Disorder in Canadian University Students
34% of first-year and 22.1% of university students overall reported having experienced at least one panic attack during the previous year (vs. more than 25% of general population at some point in life)
Those meeting criteria for panic disorder had 4 attacks on average over the previous year
What are the comorbidity of panic disorders
PD has been linked with a wide range of conditions, including depression, GAD, alcohol and drug use, and personality disorders (Cluster C)
also linked with physical conditions such as asthma
Etiology of panic disorder - biological factors
Physical illness symptoms may sometimes contribute to the development of panic disorder e.g.,
Mitral valve prolapse syndrome - heart palpitations
Inner ear disease - dizziness
PD may be tied to feeling of suffocation
Brains of those with panic disorder may have a low threshold for detecting decreased oxygen in the blood
e.g. PD patients cannot hold their breath as long as control participants
What is the genetic component of panic disorders
Genetic Diathesis
Panic disorder runs in families and has greater concordance in identical-twin pairs than in fraternal twins and increased risk of 5–16% among relatives of those with panic disorder
Which neurotransmitters are implicated in panic disorders
Norepinephrine (NE)
gamma-aminobutyric acid (GABA)
cholecystokinin (CCK): induces anxiety-like symptoms in rats that can be blocked with benzodiazepines
Etiology of panic disorder - cognitive theories
high physiological arousal (e.g., rapid heart rate) = a sign of great danger – misinterpretation of bodily sensations
repeated occurrences LEAD TO worrying excessively = panic attacks are more likely
“The result is a vicious circle: fearing another panic attack leads to increased autonomic activity; symptoms of this activity are interpreted in catastrophic ways; and these interpretations in turn raise the anxiety level, which eventually blossoms into a full-blown panic attack”
Describe the findings of the Telch and Harrington article on panic disorders
The frequency of panic attacks was strikingly high in participants who feared their bodily sensations, breathed air containing a high concentration of carbon dioxide, and did not expect it to be arousing
80% of the group with no control had a panic attack, compared with only 20% of those who thought they could control CO2 levels. The findings demonstrate the importance of perceived control in panic disorder
Panic disorder - biological treatments
treatment of choice - SSRIs, but also tricyclics, monoamine oxidase inhibitors (MOIs), and benzodiazepines
self-medication with anxiolytics or alcohol
self-medication linked with suicidal ideation and suicide attempts
Panic disorder - cognitive treaments
3-step approach
1. education & cognitive restructuring (e.g., correcting misinterpretation of bodily sensations)
2. relaxation training
3. exposure to the internal cues that trigger panic (e.g., jumping, running)
CBT treatments show better results in long-term follow-ups than tricyclics, MAOI, and benzodiazepines
mindfulness-based cognitive therapy (MBCT)
Describe General Anxiety Disorder (GAD)
persistent anxiety, often about minor items (e.g., being late for appointments, having too much work to do etc.) uncontrollable in nature other features of GAD: difficulty concentrating tiring easily restlessness and irritability high level of muscle tension Symptoms must last for 6 months for DSM diagnosis
Describe the prevalence, onset and comorbidity of GAD
lifetime prevalence - 4.2% for men and 7.1% for women
onset typically in mid-teens
stressful life events may contribute to GAD’s onset
high level of comorbidity with other anxiety disorders and with mood disorders
difficult to treat
Etiology of GAD: The Sociocultural Perspective
most likely to develop in people faced with social conditions that are dangerous
example: Hurricane Katrina in 2005, Haiti earthquake in 2010, etc.
one of the most powerful forms of societal stress is poverty
run-down communities, higher crime rates, fewer educational and job opportunities, and greater risk for health problems
there are higher rates of GAD in lower SES groups
societal interventions critical
Etiology of GAD: Behavioral views
Behavioral model of GAD is identical to one of the learning views of phobias - the anxiety is regarded as having been classically conditioned to external stimuli, but with a broader range of conditioned stimuli
Etiology of GAD: Cognitive Perspective, old school
Initially, theorists suggested that GAD is caused by maladaptive assumptions
Albert Ellis identified basic irrational assumptions:
1. It is a dire necessity for an adult human being to be loved or approved of by virtually every significant person in his community
2. It is awful and catastrophic when things are not the way one would very much like them to be
When these assumptions are applied to everyday life and to more and more events, GAD may develop
Etiology of GAD: Cognitive Perspective, nowadays (3)
- Metacognitive theory
Developed by Wells; suggests that the most problematic assumptions in GAD are the individual’s worry about worrying (meta-worry) - Avoidance theory
Developed by Borkovec (1998) - worrying serves a “positive” function for those with GAD by reducing unusually high levels of bodily arousal and other fears. Has has shown that worry is actually negatively reinforcing; it distracts people from negative emotions… - Intolerance of uncertainty theory
Certain individuals consider it unacceptable that negative events may occur, even if the possibility is very small; they worry in an effort to find “correct” solutions
CBT therapies for GAD (2)
- exaggerated exposure to the source of one’s overly anxious concern (e.g., a person worried about why his or her spouse is late coming home from a trip…)
Two processes are assumed to operate here to reduce worry:
because the client remains in a fearsome situation, anxiety is believed to extinguish
by considering the unlikelihood of the worst fears imagined, the client alters his or her cognitive reactions to his or her spouse’s not showing up when expected
E.g. someone imagine their spouse is late, then imagine the worst case scenario and stay in that fear for as long as possible. When the fear diminishes, the therapist would ask for alternative explanations - Changing maladaptive assumptions -Ellis’s rational-emotive therapy (RET)
Point out irrational assumptions
Suggest more appropriate assumptions
Assign related homework
Studies suggest at least modest relief from treatment
Mindfulness based therapies for GAD
Breaking down worrying
Therapists begin by educating clients about the role of worrying in GAD and have them observe their bodily arousal and cognitive responses across life situations
In turn, clients become increasingly skilled at identifying their worrying and their misguided attempts to control their lives by worrying
With continued practice, clients are expected to see the world as less threatening, to adopt more constructive ways of coping, and to worry less
Research has begun to indicate that a concentrated focus on worrying is a helpful addition to traditional cognitive therapy
GAD: The Psychodynamic Perspective
Freud believed that all children experience anxiety
1. Realistic anxiety when they face actual danger
2. Neurotic anxiety when they are prevented from expressing id impulses
3. Moral anxiety when they are punished for expressing id impulses
The impulses, usually sexual or aggressive in nature (id), are struggling for expression (neurotic anxiety), but the ego cannot allow their expression because it unconsciously fears that punishment will follow (moral anxiety) = GAD
Since the source of the anxiety is unconscious, the person experiences apprehension and distress without knowing why
The person with a phobia may be regarded as more fortunate, since his or her anxiety is displaced onto a specific object or situation, which can then be avoided
Psychoanalysts work to help clients confront the true sources of their conflicts. Treatment is much the same as that for phobias.
GAD: The Humanistic-Existential Perspective
Carl Rogers’s explanation:
Lack of “unconditional positive regard” in childhood leads to “conditions of worth” (harsh self-standards)
These threatening self-judgments break through and cause anxiety, setting the stage for GAD to develop
Practitioners try to show unconditional positive regard for their clients and to empathize with them
Existential approaches emphasize the need for authenticity, facing life choices, making meaning
GAD: Biological treatments
Biofeedback
Therapist uses electrical signals from the body to train people to control physiological processes
Electromyograph (EMG) is the most widely used; provides feedback about muscle tension
Found to have a modest effect
Historically – anxiolytics
Barbiturates; e.g. barbital (Veronal) and pentobarbital (Nembutal)
Benzodiazepines; e.g., diazepam (Valium) and alprazolam (Xanax)
Currently - a wide range of drugs, including
Benzodiazepines
Second generation anxiolytics (e.g., buspirone)
Antidepressants - SSRIs, SNRIs (e.g., duloxetine is seemingly effective - Ryan et al., 2008)
Atypical antipsychotics (Davidson, 2009)
Antihistamines
What are the benefits of second-generation anxiolytics
treat depression that often accompanies anxiety
no sedation, confusion, or mental clouding
no enhancement of CNS-depressant effects of alcohol or other depressants
no potential for recreational use or dependence
no withdrawal syndrome
What is in the new chapter of the DSM-5 regarding OCD
OCD hoarding disorder body dysmorphic disorder excoriation (skin-picking) disorder trichotillomania (hair-pulling disorder)
a separate category created because OCD differs considerably from other anxiety disorders (repetitive behaviors, inability to resist impulses and urges etc.)
deleting the requirement that people recognize their obsessions or compulsions as excessive or unreasonable (same specifier for body dysmorphic and hoarding disorders)
thus, the lack of insight/delusional beliefs warrants a diagnosis of the relevant obsessive-compulsive or related disorder, rather than a schizophrenia spectrum or other psychotic disorder
Describe the prevalence, onset, and demographics of OCD
Lifetime prevalence of 1-2% ; consistent across countries .
Early onset (before 10) - associated with comorbid tic and Tourette’s disorders
Early onset - more common among men (often checking compulsions);
Later onset - more frequent among women (linked to cleaning compulsions)
Typically greater impairment than anxiety or stressor-related disorders
It’s been argued that OCD is different from compulsive gamblers, compulsive eaters, and compulsive drinkers
Describe the obsessions in OCD
intrusive, uncontrollable and recurring thoughts, impulses, and images
interfere with normal functioning
the most frequent obsessions - fears of contamination, fears of expressing some sexual or aggressive impulse, etc.
can take the form of extreme doubting, procrastination, and indecision.
Describe the compulsions in OCD
Repetitive behaviors or mental acts that the person feels driven to perform to reduce the distress caused by obsessive thoughts or to prevent some calamity from occurring
The activity is not realistically connected with its apparent purpose and is clearly excessive
Give examples of commonly reported compulsions:
checking, verifying that already performed acts were actually carried out
pursuing cleanliness and orderliness, sometimes through elaborate ceremonies that take hours and even most of the day
avoiding particular objects, such as anything brown
performing repetitive, magical, protective practices, such as counting, saying certain numbers, or touching a talisman or a particular part of the body
performing a particular act, such as eating extremely slowly
Name 5 types of obsession from OCD and its related compulsions
- Contamination –> washing
- Order –> ordering
- Losing control –> counting
- Doubt –> checking
- Possible need –> hoarding
Etiology of OCD: Behavioural and Cognitive theories
learned behaviors reinforced by fear reduction
anxiety, as measured by self-reports, and psychophysiological responses can indeed be reduced by compulsive behaviors
it has also been proposed that compulsive checking results from a memory deficit, however evidence is equivocal
Cognitive Explanation of OCD – thought-action-fusion
(1) the mere act of thinking about unpleasant events increases the perceived likelihood that they will actually happen
(2) at a moral level, thinking something unpleasant (e.g., imagining the self hurting others) is the same as actually having carried it out.
some characteristics of intrusive thoughts from OCD
thoughts are especially upsetting if they are inconsistent with valued aspects of the self
consequences of actively suppressing intrusive thoughts – “thinking about the white bear” experiments
Biological Factors of OCD
The prevalence of OCD is higher among the first-degree relatives of OCD clients (10.3%) than in control relatives (1.9%) (Pauls et al., 1995)
Encephalitis, head injuries, and brain tumors have all been associated with the development of OCD (Jenike, 1986)
Interest has focused on four areas of the brain that could be affected by such trauma:
frontal lobes
striatum/basal ganglia (caudate, putamen, globus pallidus)
thalamus
amygdala
Which neurotransmitters are involved in OCD (4)
- Glutamate
- Serotonin
- Dopamine
- GABA
Which structures are believed to be involved in OCD (3)
- Cortex
- Striatum
- Thalamus
What did neuroimaging studies found on OCD
increased volume and metabolism of the caudate nucleus have been consistently associated with OCD; e.g., exposure to adverse childhood experiences was associated with increased, and ongoing drug treatment with decreased, caudate gray matter in OCD
note: these results do not allow for any causal relationships to be established
Biological Treatment of OCD
SSRIss and some tricyclics – used most often (however effective only for a selected proportion of people with OCD – 40-60%;
the symptoms usually return when the drugs are discontinued (see Jenike, 2004)
if medication and behavioral treatments are not effective, transcranial magnetic stimulation (TMS) may be used
psychosurgery – cingulotomy - involves destroying two to three centimeters of white matter in the cingulum (treatment of last resort, given its permanence, the risks of psychosurgery, and the poor understanding of how it works)
Therapies for OCD – behavioral
OCD is one of the most difficult psychological problems to treat
Exposure and response prevention (ERP) - the most widely used and generally accepted behavioral approach to compulsive rituals, pioneered by Meyer (1966)
typically involves exposures lasting 90 minutes or longer for 15 to 20 sessions within a 3-week period (with practice/homework between sessions)
CBT for OCD
focus on modification of dysfunctional beliefs involving the sense of personal responsibility etc.
group CBT/ERP for OCD may be also effective (in fact better results were achieved by group CBT relative to pharmacological treatment in a few studies
Psychoanalytic Theory on OCD
Anxiety disorders develop when children come to fear their id impulses and use ego defense mechanisms to lessen their anxiety
OCD differs from other anxiety disorders in that the “battle” is not unconscious (typically); it is played out in overt thoughts and actions
Id defenses = counter-thoughts or compulsive actions
Sigmund Freud believed that OCD was related to the anal stage of development
Alfred Adler viewed OCD as a result of feelings of incompetence (e.g., when children are kept from developing a sense of competence by excessively dominating parents)
There is little empirical support for these theories
Name 3 types of symptoms from schizophrenia
Positive symptoms (e.g. hallucinations, delusions)
Negative symptoms
(e.g. blunted affect, social withdrawal)
Disorganized symptoms
(e.g. speech, thought, and behavior)
Name the main features of schizophrenia
complex psychiatric disorder
major disturbances in attention, perception, emotion, motivation, motor behavior, language, thought processing
What are the suicide rates of people with schizophrenia
often poor outcome and decreased quality of life
suicide rate - about 10-15% (50% attempted)
How did Kraepelin describe schizophrenia
1898 – Emil Kraepelin - differentiated two major groups of endogenous psychoses:
manic-depressive illness
dementia praecox
Dementia praecox included:
dementia paranoides
catatonia
hebephrenia
Kraepelin believed that they shared a common core: an early onset (praecox) and a deteriorating course marked by a progressive intellectual deterioration (dementia)
How did Bleuler describe schizophrenia
1908 - Eugen Bleuler – argued that:
the disorder did not necessarily have an early onset
it did not inevitably progress toward dementia
and thus proposed his own term, schizophrenia, from the Greek words schizein, meaning “to split,” and phren, meaning “mind,” to capture what he viewed as the essential nature of the condition -“breaking of associative threads”
prevalence, onset, course etc. of schizophrenia
lifetime prevalence - is generally accepted to be about 1% though estimates vary from 0.2 to 2%
onset - usually appears in late adolescence or early adulthood
course - number of acute episodes with less severe but still potentially very debilitating symptoms in-between
sex/gender differences (onset, symptomatology, treatment response)
comorbidity with substance abuse, mood disorders, anxiety as well as personality disorders
sex/gender differences in schizophrenia
men - poorer premorbid functioning & earlier age at onset
men - more negative symptoms (e.g., social withdrawal, blunted affect, avolition)
women – more affective symptoms (e.g., dysphoria, inappropriate affect, impulsivity)
remission and recovery rates of schizophrenia
Menezes et al. (2006) performed a meta-analytic review of longitudinal outcome studies of first-episode psychosis and concluded that a good/remitted outcome occurred in 42% of clients, whereas a poor/chronic outcome was found in 27%
Remschmidt et al. (2007) reported on outcomes for childhood-onset schizophrenia and concluded that only 16% had a good outcome, 24% had a moderately improved outcome, and 60% had a poor outcome.
Long-term prognosis follows the rule of thirds:
One third of patients improve significantly
One third basically stay the same
One third become chronically and severely disabled
SZ and comorbidity
personality disorders (most common - avoidant, dependent, antisocial)
substance abuse and dependence (especially alcohol and cannabis)
mood (major depressive disorder) and anxiety disorders (particularly social phobia), as well as OCD and PTSD
SZ and violence
Most patients rarely engage in violent behavior
Risk factors for violence are:
Being male
Comorbid substance abuse
Not taking medication
Having engaged in criminal behavior or a history of psychopathic tendencies before schizophrenia developed
Those with schizophrenia are more likely to be victims of violence rather than perpetrators
Clinical symptoms of SZ
The presentation, course, and outcome are variable and diverse, e.g.:
some start with delusions but no hallucinations; others become isolated socially and show positive symptoms only later
some have history of poor social and academic adjustment that predate their illness; others seem to have thrived until stricken suddenly with their first psychotic episode
OVERALL - there are no specific traits or characteristics that are shared by all persons with the diagnosis
Positive symptoms of SZ
Positive symptoms - excesses or distortions, e.g., hallucinations, delusions, disorganized speech and behavior (note: disorganized speech and behavior are sometimes included under a separate symptom cluster called ‘disorganization’; Liddle et al; 1998)
defined, for the most part, as acute (psychotic) episode of schizophrenia
Hallucinations
Vivid sensations that seem real, but are not
Occur in all senses – auditory are most common
Delusions
Persistent false beliefs, held despite evidence to the contrary
Focus on a particular theme
Name 4 types of delusions in SZ
Paranoid delusions – persecution by others
Delusions of control – being controlled by others, who put thoughts into one’s head (thought insertion)
Delusions of grandeur - belief that one is more powerful, knowledgeable, or capable than is actually the case
Delusions of reference - belief that external events have special meaning for the individual
Describe delusion of control in SZ
The person may be the unwilling recipient of bodily sensations or thoughts imposed by an external agency
People may believe that their thoughts are broadcasted or transmitted, so that others know what they are thinking
People may believe that their thoughts are being stolen from them, suddenly and unexpectedly, by an external force
Some people believe that their feelings are controlled by an external force
Some people believe that their behavior is controlled by an external force
Some people believe that impulses to behave in certain ways are imposed on them by some external force
Describe hallucinations in SZ
Some people with schizophrenia report hearing their own thoughts spoken by another voice
Some people claim that they hear voices arguing
Some people hear voices commenting on their behavior
Name 6 types of disorganized speech in SZ
Also known as formal thought disorder due to:
1. Loose associations
2. Derailment (different from digressing, no return)
3. Neologisms (made-up words)
4. Perseveration (patients repeat their words and statements again and again
5. Word salad
6. Clang (rhymes):
How are you? “Well, hell, it’s well to tell”
How’s the weather? “So hot, you know it runs on a cot”
However disorganized speech is not present in all the patients with SZ and it does not discriminate well between schizophrenia and other psychoses, such as some mood disorders (Andreasen, 1979)
Describe disorganized behavior in SZ
So unfocused and disconnected from a goal that tasks cannot be accomplished
Inappropriate and/or incongruent with a situation (often accompanied by inappropriate affect)
Catatonia: Condition in which an individual remains in an odd posture or position, with rigid muscle, for hours
Describe 5 negative symptoms of SZ
Absence or reduction of normal mental processes and behaviors
- Avolition: difficulty in initiating or following through with activities
lack of energy - Alogia: poverty of speech (amount and content)
responding slowly and/or minimally to questions - Flat Affect: Narrowed range of emotional expression
Emotionally neutral, refrain from making eye contact
Experience emotion, but not apparent from casual observation - Anhedonia: lack of interest in recreational activities, relationships with others and sex
- Asociality: Few friends, poor social skills, and little interest in being with others
Describe neurocognitive symptoms of SZ
Cognitive deficits (similar to what we see in ‘frontal deficit’ patients)
attention
working memory
executive functioning
Mental processes involved in planning, organizing, problem solving, abstract thinking, and exercising good judgment
Required to organize, interpret, and transform information in working memory
For some, cognitive deficits existed in childhood, long before first episode of schizophrenia
Deficits persist even when positive symptoms lessen or stop
Name similar disorders to schizophrenia
Many disorders may present similarly to schizophrenia, including:
Mood disorders
Substance-related disorders
Psychotic disorders
Schizophreniform and brief psychotic disorders
Schizoaffective disorder
Delusional disorder
Schizotypal personality disorder (categorized as a personality disorder, rather than psychotic disorder)
Mood Disorders and Substance-Related Disorders
May involve hallucinations and delusions
Usually consistent with characteristics of the disorder
Only arise during a mood episode or with substance use or withdrawal
Psychotic mania distinguished from schizophrenia by presence of other symptoms of mania
Pressured speech or little or no need for sleep
Substance-related disorders can lead to delusions and can induce hallucinations
Negative symptoms often difficult to distinguish
Depressive symptoms can be similar
Those with schizophrenia typically do not have other depressive symptoms, e.g., weight changes, feelings of worthlessness
What is Schizophreniform disorder
Symptoms that meet all the criteria for schizophrenia
Symptoms have been present for only 1-6 months
Daily functioning may or may not have declined over that period of time
What is Brief psychotic disorder
Sudden onset of positive or disorganized symptoms
Lasting between a day and a month and followed by a full recovery
What is Schizoaffective disorder
Presence of both schizophrenia and a depressive, manic, or mixed mood symptoms
DSM-5 addition - a major mood episode must be present for a majority of the time the disorder has been present in the person
Name 5 subtypes of delusional disorder
Delusional disorder- presence of non-bizarre (or bizarre in DSM-5) but demonstrably incorrect beliefs that have lasted for more than 1 month
Erotomanic – belief that another person is in love with patient
Grandiose – belief that the patient has great (but unrecognized) ability, talent, etc.
Persecutory – belief that the patient is being spied on, drugged, harassed, or conspired against
Somatic – false belief that bodily sensations indicate some abnormality or that there is a bodily malfunction
Jealous – belief that the patient’s partner is unfaithful
What is Schizotypal Personality disorder
May actually be a milder form of schizophrenia
Problems in relationships may become evident in early adulthood
Marked by discomfort when relating to others and being stiff or inappropriate in relationships
Eccentric behavior, such as difficulty following social conventions, is also present
Does not involve psychosis
What is folie à deux
Shared psychotic disorder, or folie à deux, is a rare delusional disorder shared by 2 or, occasionally, more people with close emotional ties. An extensive review of the literature reveals cases of folie à trois, folie à quatre, folie à famille (all family members), and even a case involving a dog (?!)
DSM-5 no longer separates delusional disorder from shared delusional disorder
What is the genetic data of SZ
A convincing body of literature indicates that a predisposition to schizophrenia is transmitted genetically
relatives of people with schizophrenia are at increased risk, and the risk increases as the genetic relationship between proband and relative becomes closer
however, a common “deviant” environment rather than common genetic factors could account for the concordance rates.
MZ twins are 44% more at risk of developping SZ, spouse 1%
Biochemical Factors, Dopamine in SZ
One of the earliest neurochemical theories of SZ proposed that it is related to increased activity of DA
first-generation (typical/conventional antipsychotics) decreased dopamine activity by blocking D2 receptors
Also produce side effects similar to Parkinson’s disease which is caused in part by decreased dopamine
Other clues provided by amphetamine psychosis
Closely resembles paranoid schizophrenia and can exacerbate symptoms of schizophrenia
Amphetamines cause release of dopamine and norepinephrine
However, the major metabolite of dopamine, homovanillic acid (HVA), was not found in greater amounts in people with schizophrenia, implying that it may be an excess or oversensitive dopamine receptors, rather than the level of dopamine itself, that play a critical role…
Subsequent developments – DA imbalance hypothesis SZ
Typical antipsychotics improve only positive symptoms (indeed amphetamine may ameliorate some negative symptoms and cognitive deficits) and produce extrapyramidal side effects (EPS such as Parkinsonism via blocking of nigrostriatal DA pathway from substrantia nigra to dorsal stratum)
Thus Davis (1991) expanded the DA theory by recognizing functional differences among the neural pathways that use dopamine as a transmitter
Which 2 DA pathways may be involved in SZ
mesolimbic pathway - from ventral tegmental area (VTA, in the midbrain) to ventral striatum (nucleus accumbens) – excess DA activity in SZ (D2 receptors) – positive symptoms
mesocortical (VTA to PFC) – diminished DA activity in SZ (D1 receptors) – negative symptoms
Serotonin in SZ
LSD model of SZ
atypical antipsychotics (e.g., clozapine) block selective serotonin receptors (e.g., 5-HT2A
5-HT neurons regulate DA neurons in the mesolimbic pathway (and vice versa)
Antipsychotic drugs in SZ (first-generation/typicals/neuroleptics/classic antipsychotics
“neuroleptic” refers to the ability of a drug to cause a syndrome known as “neurolepsis”:
Psychomotor slowing
Emotional quieting
Affective indifference
Classic FGA are D2 antagonists and include
phenothiazines (e.g. chlorpromazine)
non-phenothiazines (e.g., haloperidol)
Side effects of FGA (first generation antipsychotic)
Extrapyramidal side effects: resemble the symptoms of Parkinson’s disease (tremors of the fingers, a shuffling gait, drooling)
Akathisia: is an inability to remain still
Dystonia: a state of muscular rigidity, and dyskinesia, an abnormal motion of voluntary and involuntary muscles, producing chewing movements, as well as other movements of the lips, fingers, and legs
Tardive dyskinesia: mouth muscles involuntarily make sucking, lip-smacking, and chin-wagging motions
Neuroleptic malignant syndrome: muscle rigidity, fever, delirium, etc.
Antipsychotic drugs in SZ (second-generation/atypicals)
“atypical” based on the view that SGAs have atypical properties, such as low risk of extrapyramidal symptoms (EPS)
As FGA block D2, but also 5HT2A receptors hence sometimes called
dopamine-serotonin antagonists, e.g.:
clozapine (for treatment resistant SZ, but risk of agranulocytosis)
risperidone
olanzapine
ziprasidone
no EPS but increased risk of developing metabolic side effects:
hyperglycemia,
weight gain etc.
no evidence that SGAs are significantly more effective than FGAs in the treatment of cognitive and negative symptoms
Side effects of FGA & SGA neuroendocrine disturbances
Under normal conditions, DA inhibits prolactin release from the pituitary via tuberohypophyseal DA pathway, which regulates pituitary hormone secretion
By blocking D2 receptors, neuroleptics stimulate prolactin secretion, which leads to lactation and breast enlargement, even in males
Overall: neuroendocrine effects include decreased sex drive, no menstruation, increased prolactin release, and inhibition of growth hormone release
Weight gain and inability to regulate body temperature are also problematic
Congenital and developmental considerations of SZ
1957, Helsinki – an epidemic of influenza virus- exposure to the virus early to mid-gestation (1st and 2nd trimester of pregnancy – increased rates of SZ in offspring (Mednick et al., 1994; Brown et al., 2004)
Brown & Derkits (2010) -suggest that prenatal exposure to infections, including influenza, rubella, and toxoplasmosis (an intracellular parasite), and maternal cytokines (known to mediate the host response to infection), are associated with increased risk of schizophrenia
Explain the Avatar Therapy for SZ
Video
treatment guidelines for schizophrenia recommend:
1 -Selection and application of antipsychotic medication to control acute psychotic symptoms, including strategies for maintaining adherence
2- Identification and treatment of comorbid disorders, including substance use and depressive disorders
3- Use of psychosocial treatment approaches with demonstrated effectiveness in improving symptoms and ability to function socially and vocationally, e.g.
family interventions/psycho-education
social skills training
CBT
assertive community treatment
supported employment
Unfortunately, few of the psychosocial treatments are used
R.D. Laing’s view + “OPEN DIALOG” model
One of the more controversial explanation of schizophrenia
Argues that the disorder is actually a constructive process in which people try to cure themselves of the confusion and unhappiness caused by their social environment
Laing believed that, left alone to complete this process, people with schizophrenia would indeed achieve a healthy outcome
Most theorists and clinicians reject this notion; research has largely ignored it…
What is the history of PTSD in the DSM
As far back as the American civil war “irritable heart”
WWI soldiers suffered from “shell shock” or “soldier’s heart”
1980, PTSD is added to DSM-III
Lumped into anxiety disorders category in DSM-IV
2013, PTSD is placed in new Trauma-and Stressor-Related Disorders forDSM-V
Diagnosing PTSD
Anyone who has suffered trauma could develop PTSD, but not everyone does Risk factors Resilience factors Physical exam first Go through a psychological evaluation Use the DSM-V criteria checklist
What is Delayed Expression in PTSD
Delayed expression: If the full diagnostic criteria are not met until at least 6 months after the event.
Name the criteria for PTSD (8)
A: Stressor criterion (experiencing traumatic event)
B: Intrusive recollection criterion (recurrent, involuntary and distressing memories)
C: Avoidance criterion (efforts to avoid the distressing memories)
D: Negative cognitions and mood criterion (Inability to remember, exaggerated negative beliefs about one’s self)
E: Alterations in arousal or reactivity criterion (irritable behaviors)
F: Duration criterion (at least 1 month)
G: Functional significance criterion (significant impairment)
H: Exclusion criterion (not attributable to physiological effects, or substance)
What is the most successful treatment of PTSD
The most successful interventions are cognitive-behavioral therapy (CBT) and medication.
Benzodiazepines and SSRIs
CBT: thoughts –> emotions –> behaviors –> physical sensations –> thoughts (and so on)
What are dissociative disorders?
Characterized by a disruption of and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behavior. Dissociative symptoms can potentially disrupt every area of psychological functioning.
Name three brief milestones in the history of DID
- Believed to be caused by demonic possession
- Labelled as hysteria and schizophrenia
- Labelled as multiple personality disorder in 1882
What are 3 myths about DID
- Communication with alters happens by seeing them outside of you and talking with them just like regular people (hallucination), possibly but very rare
- You can ‘kill’ alters
- Integration is a ‘must’, everyone’s goal in therapy
Psychodynamic Model of DID
repression and compartmentalization
“Dissociative disorders are caused by an individual’s repressed thoughts and feelings related to an unpleasant or traumatic event”
CONTROVERSY: The Sociocognitive model of dissociative identity disorder
DID is not a valid psychiatric disorder of posttraumatic origin; rather, it is a creation of psychotherapy and the media.
Treatment recommendations for DID
- Medication
- Psychotherapy
- Hypnosis
What is Dissociative Identity Disorder
- Disruption of identity characterized by two or more distinct personality states.
- Recurrent gaps in the recall of everyday events
- Cause clinically significant distress
- Not a religious practice
- Not due to substance abuse
What is the difference between DID and schizophrenia
The personified, internally communicative inner voices of DID may be mistaken for psychotic hallucinations. DID experience symptoms as caused by alternative identities, but do not have delusional explanations for the phenomena
