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69 Cards in this Set
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Endophenotype |
a hereditary characteristic that is normally associated with a condition (i.e. vulnerability for a condition) but is not a direct symptom of that condition (e.g. rumination) |
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Bipolar II (briefly) |
characterized by hypomanic and major depressive episodes (hypomania is not severe enough to cause marked impairment, no psychotic features, but must last at least 4 days, show change in functioning, and be observable by others). Data support the view that bipolar II is a distinct condition, though has some overlap with bipolar I and MDD
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Cyclothymia (briefly) |
a mild form of bipolar disorder in which a person has mood swings over a period of years that go from mild depression to emotional highs. Episodes of hypomania and mild depression must occur for at least two years. Mood swings are less severe than bipolar. Sxs are persistent and no more than 2 months sxs free in a row
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Negative Cognitive Triad |
“pessimistic views about the self, the world, and the future” (Joorman, 2009)
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Schemas (memory representations) |
help individuals make sense of their environment by guiding individuals towards information that makes sense according to their schemas. Beck says that the schemas of depressed individuals include negative themes (e.g. loss, failure, worthlessness) so that they only pay attention to the negative stimuli around them, or if something is neutral, they would interpret it negatively. These dysfunctional schemas are activated by stressors and negative cognitions become automatically revolved around negative views of the self, world and future.
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Cognitive distortions |
exaggerated or irrational thoughts, such as: 1. All-or-nothing thinking 2. Overgeneralization 3. Mental filter 4. Disqualifying the positive 5. Jumping to conclusions (Mind reading, The fortune teller error) 6. Magnification (catastrophizing) or minimization 7. Emotional reasoning 8. Should statements 9. Labeling and mislabeling 10. Personalization
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Affective interference |
The affective interference hypothesis posits that because depressed persons are preoccupied with processing emotional material, their performance on other tasks will not be impaired if they need to process emotional aspects of stimuli, but it will suffer if they have to ignore emotional aspects and respond to other aspects of material. Thus, since depressed individuals are preoccupied with noticing negative aspects of stimuli, it is difficult for them to solely process other aspects of material without noticing the emotional (usually perceived as negative) material associated with the stimuli.
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Anxiety disorders (list) |
1. Obsessive Compulsive Disorder (OCD) 2. Generalized Anxiety Disorder (GAD) 3. Posttraumatic Stress Disorder (PTSD) 4. Agoraphobia 5. Panic Disorder (PD) 6. Anxiety due to Medical Condition 7. Phobias (specific) 8. Social Phobia 9. Substance-induced Anxiety Disorders
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Mood disorders (list) |
1. Major Depressive Disorder 2. Dysthymic Disorder 3. Bipolar I Disorder 4. Bipolar II Disorder 5. Substance-induced Mood Disorder 6. Mood Disorder due to a General Medical Condition 7. Adjustment Disorder with Depressed Mood 8. Cyclothymic disorder
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Agoraphobia (briefly) |
Anxiety about being in places or situations from which escape might be difficult or in which help may not be available in the event of having an unexpected or situationally predisposed Panic Attack or panic-like symptoms. Agoraphobic fears typically involve characteristic clusters of situations that include being outside the home alone (open spaces): being in a crowd or standing in a line, being on a bridge, and traveling in a bus, train, or car.
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Compulsive hoarding |
A disorder characterized by the excessive collection of items (that often appear to be of little or no use to other people) and an inability to throw them away to the point where parts of one’s home can no longer be used for their intended purpose. It may (should) cause significant distress or impairment. May be a symptom of OCD but many people who hoard don’t have OCD symptoms and hoarding can be found in people with neuropsychiatric disorders like dementia, psychotic disorders, eating disorders, autism and also in people with no psychiatric disorders.
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Separation anxiety disorder |
Developmentally inappropriate and excessive anxiety (so severe it looks like a panic attack) concerning separation from home or from those to whom the individual is attached, as evidence by THREE or more of the following. Has to last at least 4 weeks and occur before the age of 18. Occurs more often in girls: 1. Recurrent excessive distress when separation from home or major attachment figure occurs or is anticipated 2. Persistent and excessive worry about losing, or about possible harm befalling, major attachment figures 3. Persistent and excessive worry that an untoward event will lead to separation from a major attachment figure (e.g., getting lost or kidnapped) 4. Persistent reluctance or refusal to go to school or elsewhere because of fear of separation 5. Persistently and excessively fearful or reluctant to be alone or without major attachment figure at home of without significant adults in other settings. 6. Persistent reluctance or refusal to go to sleep without being near a major attachment figure or to sleep away from home 7. Repeated nightmares involving the theme of separation 8. Repeated complaints of physical symptoms (headaches, stomachaches, nausea, or vomiting) when separation from major attachment figures occurs or is anticipated.
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Separation anxiety disorder brief |
A disorder of childhood characterized by obvious distress when separated from an attachment figure. Also overly demanding, clingy, and refusal to let go. Distress can be so severe that it can lead to panic attack-like symptoms. Has to cause an impairment in functioning (e.g., school refusal).
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Obsessions |
Recurring thoughts that crop up randomly and are beyond a person’s control. Once an obsessive thought begins, the person is generally unable to get rid of the thought. Usually is disruptive and causes distress.
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5 HT |
Shorthand for the chemical name of serotonin. Mutations in genes related to 5 HT cause dysfunction with serotonin and/or the receptors. Serotonin dysfunction can lead to many different symptoms, and is likely a factor in several different mental disorders. Discuss as a gene related to serotonin. So that means, it affects the proteins related to serotonin reuptake or the effectiveness of serotonin.
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COMT |
gene investigated in relation to schizophrenia. Purpose is to regulate protein development that dictates dopamine levels in the prefrontal cortex, also related to epinephrine and norepinephrine levels. Originally investigated because of association with prefrontal cortex dopamine levels, current research (Stefanis et al 2007 study with Greek men in military) has found that certain polymorphisms on the gene (specifically 2 short alleles) are related to increased risk of schizophrenia in the presence of stress.
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Panic attacks |
sudden discrete episode of very intense anxiety, usually accompanied by feelings of doom. Panic attacks are very common in community samples. Part of their diagnostic criteria is that they are supposed to be unexpected but they might not be in reality.
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Conversion disorder |
loss of motor or sensory functioning not corresponding to any medical findings or neurological pathways disruptions, demonstrates a disconnect between body and mind. Often seen as loss of sight, hearing, motor abilities or as neurological symptoms such as non epileptic seizures.
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Describe the major boundary issues involved in major depressive disorder. |
1. vs. schizoaffective disorder: psychotic features with mood problems with mood problems original to the psychosis. 2. vs. MDD with psychotic features, in which depression comes first. need to think: which one is driving? need to have psychotic sxs in absence of mood problems for at least two weeks, overlap with paranoia/thinking that no one likes you 3. vs. normal sadness/depression: mild depression responds equally well to placebo and SSRIs (both result in slight improvement), evidence that depressive disorders are on a continuum 4. vs. anxiety 5. vs. grief: defined as due to death of a loved one, but doesn’t include job loss, divorce, etc., also only given 2 months 6. (in bipolar): mania vs. normal good mood 7. boundary between personality and psychopathology
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What are the age and gender differences in onset and prevalence of major depressive disorder? |
ranges in estimates of prevalence depending on sampling strategy (community vs. clinical, what you assess)
o 2:1 ratio of women:men with MDD across countries o point prevalence: 9% of women and 4% of men o differences start to appear after age 13, start to shrink after middle age o MDD is less common in younger kids, increases with age (3% kids, 14% adolescents) o Kessler,1998 Natl. Comorbidity Study: 25% of teens met criteria for MDD by 18 years old. up to 50% met criteria for subclinical (seems high). adults: lifetime prevalence of 17%, 5% with 30 day + prevalence, highest rates ages 25 to 45 |
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Describe the evidence that supports these differences, and present a theoretical conceptualization of the pattern. |
1. Cyranowski, 2000 review: diathesis * stress model to explain gender differences 2. Casey et al, 2008: imbalance model: mood problems are triggered in adolescence due to differential timing in brain development
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Cyranowski 2000: diathesis * stress model |
diatheses: 1. biological: production of oxytocin (more in girls), related to the pursuit of affiliative relationships 2. psychosocial: “vulnerable girls,” risks: insecure parental bonds, anxious temperaments, poor task-oriented coping (rumination) 3. cycling: experiences of rejection → neediness → rejection.
Moderation approach: relationship between A & C depends on/only exists with B |
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Casey et al 2008 imbalance model: |
mood problems are triggered in adolescence due to differential timing in brain development.
Two brain systems developing: 1. limbic subcortical regions (ventral system): emotion center, fight/flight, desire 2. prefrontal cortex: top down processing, tampers things down, regulates behavior. These two systems develop at different rates: PFC at a liner rate (till age 27/28), limbic system at quadratic rate (peaks earlier in adolescence). If you combine this with diathesis, you have an additional layer of stress: 1. more oriented towards affiliative relationships AND 2. more prone to rejection |
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What is the course of major depressive disorder? When does it first onset? What is its duration? What is the prognosis, and how does prognosis relate to age of onset? |
Onset: across people, mean age is in 20s, subset of folks who develop it younger
Duration: adults: 6 months to1 year (untreated), teens/kids: 7 to 9 months (tend to remit within 2 years, lots of recurrence), community samples: 26 weeks/6 months Recovery: 1 year without sxs Recurrence: 80% with MDD history experience another episode, 40% of teens re-experience within 2 to 5 years, biggest risk factor = age of onset |
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Developmental continuity of MDD and evidence: |
mixed evidence
for: in clinical & community samples, MDD in childhood is a big risk factor for MDD in adulthood, subsyndromal sxs levels predict future sxs against: kids diagnosed with MDD experience other forms of impairment later |
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3 hypotheses for recurrence of MDD: |
1. kindling: Post (1992), early occurrences of depression increase neurobiological sensitization to the point that recurrence can be caused by neurobiology (esp. re: bipolar), brain takes over
2. stress sensitization: life stress predicts initial onset for depression, brain changes so you become more sensitive to future sxs 3. scarring: depression causes brain abnormalities that permanently disrupt neurobiological fxing (would look like stable flat line, but depression looks like waves/cycles) |
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Describe three types of gene environment correlation. Provide examples using unipolar depression. |
1. passive: child receives g & e from parent. Evidence for the heritability of stress, h2 coefficient doesn’t change depending on how you measure stress (perception vs. events). People who are depressed are 2.5x more likely to have experienced 1 or more SLEs (Shrout et al, 1989), can’t determine directionality based on this but later research supports g*e correlation
2. evocative: child elicits certain types of responses, ex: cycling from Cyranowski (2000) review: rejection → neediness → rejection 3. active: child selects, creates, & modifies environmental experiences based on genes (eg causing more stressful life events). Stronger in adolescence and adulthood than in kids. In this sense, genes become more important (how genes influence environment) ex. shyness → may not seek friends → loneliness → depression |
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Provide evidence to demonstrate gene*environment interactions in the development of Major Depressive Disorder. Describe the research and implications of the findings on the conceptualization of the disorder. |
The Kendler study, which was a replication of the Caspi study that was done on the Dunedine cohort
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Kendler study Method |
Assessed 549 twins from the Virginia Adult Twin study for MDD over the past 14 years (Longitudinal study). They also assessed for GAD over the past year.
They asked about 11 Stressful Life Events (SLEs) to the nearest month also asking about SLEs duration and perceived threat level. They analyzed their DNA for the presence of long or short alleles of the 5 HTT gene dividing participants into two groups, those who have two long alleles or one long and one short allele (SL/LL), and then those who have two short alleles (SS) |
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Kendler Study Results |
Found a significant main effect for sex and for stressful life events but not for genotype on the prediction of depression.
There was however, a significant interaction of gene by stressful life event. People who have two short alleles have an increased risk for MD following a stressful life event than people with one or more long alleles When severity of stress, (threat level) was taken into account they found that, the risk (hazard ratio) for MD increases with higher severity levels, that at all severity levels, risk is greater for females, and that at all levels of severity of stress, risk was greater for those with the two shorts (SS) than those with one or more longs (SL/LL) with a large difference at lower levels (1,2) and a much smaller difference at higher levels of stress (3,5) |
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Implications of the Kendler study findings |
Combined with the findings of the Rice et al. 2006 study, the implications are that genetic risk for the depressive phenotypes may expose teens to social adversity, making them more susceptible to get MDD in response to environmental risks. If we identify people who are genetically at risk we could intervene in their environments to reduce the negative effect that environments could have. (e.g. picking better friends or not taking drugs)
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Garber on g*e for MDD |
children with MDD are 2.3 x more likely to have first-degree relative with MDD. “Estimates of heritability tend to be moderate, shared environment effects tend to be small, and nonshared environmental effects emerge as the largest environmental influence on individual differences in childhood depression”
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What is known about the role of neurotransmitters in the development of major depression? |
1. Serotonin: 5 HTT is a gene that affects depression through affecting the proteins that affect the reuptake of the neurotransmitter serotonin. The lack of Serotonin in the system has been shown to affect levels of depression. That is why SSRIs have the ability to reduce levels of depression because they inhibit the reuptake of this neurotransmitter thereby increasing levels of it in the bloodstream and thus reducing levels of depression.
2. Studies have also shown that sensitivity to low levels norepinephrine in the prefrontal cortex increases risk of depression. This is a neurotransmitter that promotes general arousal, concentration and memory, malfunctions of which are symptoms of depression. 3. Low levels of Dopamine are also evident in people with depression. This is a neurotransmitter that responds to the feeling of rewards, or liking something, i.e. when you like something you get a rush of dopamine in the system and thus you feel good, but if you do not have enough of this substance, things you like do not give you the release of dopamine that you need and thus they seem less pleasurable |
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How does the functioning of the primary NTs relate to each other? |
serotonin, norepinephrine, & acetylcholine play a big role/possible serotoninergic system marker, SSRI effectiveness indicate that serotoninergic system dysregulation may be a risk factor [Garber..]
While each NT contributes separately to different aspects of depression, when combined they create the full picture of lowered arousal, anhedonia, and rumination/increased attention to negative stimuli. |
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How does the construct of affective interference explain the development, maintenance, and reoccurence of major depressive disorder? |
The affective interference hypothesis says that depressed people are too busy processing emotional material such that in experiments where they need to process emotional material they perform well but in experiments that require them to ignore the emotional information and respond to other aspects of the material they do not do well. This way of thinking can develop over time especially if reinforced or simply by practice because the more a person learns to pay attention to the (negative) emotional aspects of situations the more likely they are to keep doing so unless cognitive intervention takes place. That is because seeing the negative emotional side of things makes a person reason emotionally and have irrational thoughts such as all or nothing and overgeneralization, thereby maintaining their depression.
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How does the construct of rumination explain the development, maintenance, and reoccurence of major depressive disorder? |
Rumination is a way of thinking that can increase the onset and perpetuation of depression by affecting working memory. There is a limited capacity for attention and focus which limits the cognitive inhibition that has to take place in order to have goal directed behavior. When this process malfunctions, a lot of trivial information can get into the working memory. This allows connections to be made between relevant and irrelevant information, which makes for slower and less focused cognitions. This makes way for negative self focused ruminative thoughts. At as these connections continue to be made with incoming information, depression is maintained simultaneously made more likely to reoccur due to the increasing number of connections being made.
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Briefly explain how rumination may function as an endophenotype of major depressive disorders. |
Rumination is a negative style of thought, not just negative content. People may be genetically predisposed to this style of thought. A ruminative style of thought exacerbates sad moods and predicts future depressive episodes. In studies where participants with dysphoria were induced to ruminate, they endorsed more negative interpretations of hypothetical situations, generated less effective problem solving strategies and showed increased recall of negative autobiographical memories. In another study, nondepressed individuals were characterized by sustained amygdalar responses to all stimuli decayed quickly after offset, whereas depressed individuals were characterized by sustained amygdalar responses to negative words. This shows that rumination can be an endophenotype for depression because although a person may have this style of thought without being depressed but it most certainly does make them more prone to it.
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Explain the tripartite/hierarchical model of major depressive and anxiety disorders. |
(Mineka, Watson, and Clark) Structural model that strives to explain the common and distinctive features of Anx and Depression, groups symptoms into 3 basic subtypes. Affect is divided into 2 components: 1. positive affect (lack is a specific factor related to MDD) and 2. negative affect (nonspecific factor that relates to both GAD/anxiety and MDD), then 3. Autonomic arousal (shortness of breath, dizziness, etc) (specific factor related to anxiety) |
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At what age do the different anxiety disorders typically onset? What does this suggest about the developmental course of these disorders? |
1. Specific phobias: median age of onset for children is 7 yrs with spontaneous remission and recovery. Adult age of onset depends on the phobic type.
2. Social phobia: highly unlikely pre puberty, prevalence rates increase with age 3. Agoraphobia: non existent in childhood, kids have no choice about where they go 4. GAD: median age of onset is 11 years 5. OCD: sxs usually meet criteria starting in early adolescence or early adulthood This pattern would suggest that there is some cognitive component required in the development of the various anxiety disorders. It makes sense that specific phobias are the earliest onset as they require only basic logic to enact (snakes are scary, avoid snakes at all cost), whereas social phobia involves more of a fear of embarrassment which requires more elaborate thinking and understanding of other people’s perceptions, a similar cognitive component could be required for the development of agoraphobia |
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Why would exposure to childhood adversity and trauma lead to the development of posttraumatic stress or major depression? Simple answer |
The simple answer to this is because early life stress leads to increased later life stress and increased stress is correlated to increased incidence of both PTSD and MDD (both fit diathesis stress model)
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Why would exposure to childhood adversity and trauma lead to the development of posttraumatic stress or major depression? Longer answer pt. 1: MDD & Stress |
MDD and stress
stress matters particularly in combination with genes more acute stressors increase the likelihood of depression early life stressors increase the likelihood of later life stressors can also talk about 5HT |
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Why would exposure to childhood adversity and trauma lead to the development of posttraumatic stress or major depression? Longer answer pt. 2: PTSD and stress: Cascade model |
Repeated stressful events lead to changes in biology (HPA axis) which increases the likelihood of future stressful events which lead to coping and behavior problems and eventually psychological problems HPA axis: early trauma relates to dysregulation in HPA, fight or flight response stops working efficiently, this is important for later life experiences fires and stops firing at the wrong time Hippocampus and hypothalmus aren’t communicating well Reduced prefrontal context due to increased HPA activity Disruption in learning/memory, attention Increased amygdala functioning High levels of cortisol changes the development of the brain, essentially a brain killer Reduction in white matter Why would exposure to childhood adversity and trauma lead to the development of posttraumatic stress or major depression? Longer answer pt. 3: Kilpatrick Study 2007 |
5HT, same short alleles from MDD, demonstrated a gxe effect of proximity to stressful event and 2 short alleles increasing likelihood to PTSD, also low social support and short alleles lead to increased risk of PTSD
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Explain the evidence for homotypic and heterotypic continuity of anxiety disorders. What implications does this have on research, intervention, and prevention?: Overview of models and types of continuity |
Current models of childhood anxiety are downward extensions of adult models, important to determine if anxiety disorders demonstrate homotypic or heterotypic continuity
Homotypic continuity: if childhood anxiety looks the same as adult anxiety but has a different underlying causal mechanism Heterotypic continuity: childhood and adult anxiety disorders look different but have the same underlying mechanism It is important to determine whether anxiety is characterized by heterotypic or homotypic continuity as it will alter our etiology models which will affect our ability to predict and thereby intervene early. Early intervention is important in anxiety because we know that the course of the disorder is fairly chronic over time. |
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Explain the evidence for homotypic and heterotypic continuity of anxiety disorders. What implications does this have on research, intervention, and prevention?: Evidence for homotypic continuity |
Kim & Cohen 2008: Dunedin: looked at kids 11 to 32, if kids had dx at 11 it predicted dx at 32 Pine et al 1998: study done in the US with 9 to 18 year olds, followed them for 10 years, also found evidence for homotypic continuity with those who were dx with any type of anxiety disorder at time 1 being 2 to 3 times more likely to be diagnosed with anxiety disorder in adulthood Goodwin et al 2004: Christchurch NZ cohort study similar to Dunedin, found evidence for homotypic continuity of social and specific phobia Kids who were dx with specific phobia had odds ratio of 3.89 for adult dx (almost 4 times more likely) Kids who were dx with social phobia had odds ratio of 3.37 for adult dx Pine et al 1998: at 10 yr followup, kids with soc phobia dx were 3x more likely to have soc phobia as an adult |
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Explain the evidence for homotypic and heterotypic continuity of anxiety disorders. What implications does this have on research, intervention, and prevention?: Evidence for heterotypic continuity |
Pine et al 1998: at same 10 year followup found odds ratio of 1 with kid GAD dx and adult GAD dx
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Explain the etiology and maintenance of anxiety disorders from a learning theories perspective. This may be done generally or in reference to one anxiety disorder. |
When a person feels anxiety, s/he may feel relief from his/her natural response. For example, a person may avoid an anxiety provoking situation, which provides relief since the anxiety does not need to be confronted. This relief can act as a reward that promotes the further avoidance of anxiety. However, it is not necessarily that the avoidance is considered rewarding, but it may be that the perceived association between the stimulus and the outcome is confirmed. That is, the relief suggests that the situation is in fact something to be avoided. In short, the learning theory suggests that the person first has classical conditioning (i.e., situation → anxiety, so the situation becomes a conditioned stimulus). Then, by reacting to the anxiety in a way that produces relief, the person undergoes operant conditioning (since the relief is a reward, confirming the conditioned stimulus).
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What limitations exist with the theory, and what are some of the theoretical extensions needed to better capture the etiology of anxiety disorders? |
Genes cannot be ignored. As a child ages, genes become increasingly important, and the environment plays a smaller role. Therefore, the learning theory is limited in how much it can account for. To best understand anxiety, we must look at G x E to determine what predisposes a person to develop an anxiety disorder, and how the interaction with the environment actually leads to the disorder. The learning theory may not be wrong, it just does not account for the whole picture.
Other limits of theory: 1. limited effect of shared environment 2. prepared fears (CO2 studies: learning theory can help us understand the cycle of the conditioning but not the initial trigger) 3. neo conditioning model: says that a vulnerability and exposure to stress combine with the learning theory( expectations are a negative reinforcer, they lead to an escalation of fears which taps into our associative memory networks) 4. Split on GxE Lau vs Kendler, big debate in field |
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Are major depressive disorder and generalized anxiety disorder the same disorder that should be classified together, or are they separate? Use evidence from multiple domains to make your argument. Include a discussion of the implications of your position on the DSM V. Argument they’re the same |
Whether or not MDD and GAD are the same disorder with different manifestations, or two separate disorders that are related, is still a controversial topic. To support the claim that they are the same, there is a lot of overlap with the etiologies. For example, they both seem to share a lot of the same genes that predispose a person to develop either disorder. In fact, GAD shares more genes with MDD than it does with other anxiety disorders. Additionally, if exclusion criteria are ignored, there is a lot of comorbidity between the two, suggesting they are perhaps the same disorder. There is also some evidence that GAD often precedes MDD, suggesting they are on the same continuum, although this is difficult to interpret due to the exclusion criteria in DSM IV. Finally, antidepressants have also been shown to be effective for both disorders, suggesting they are operating in a similar way. To explain the discrepancies between the two, it could be explained that they are the same disorder, just with different thought patterns or thought biases (i.e., anxiety deals with fear, depression deals with loss).
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Are major depressive disorder and generalized anxiety disorder the same disorder that should be classified together, or are they separate? Use evidence from multiple domains to make your argument. Include a discussion of the implications of your position on the DSM V. Argument they’re different |
However, there is also support that they are distinct. First, detailed analysis suggests that GAD may not actually be a stepping stone toward MDD. Instead, it could be that MDD is just as likely to precede GAD as the other way around. If this is true, it suggests that each is a risk factor for the other, but that they are on different continuums. Additionally, although there are some symptoms that overlap, MDD does have some distinct features. For example, MDD is marked by chronically elevated levels of cortisol and chronically low levels of dopamine, whereas GAD only has episodic increases in cortisol and is unrelated to dopamine, suggesting the neurochemical relations of each disorder are different. Finally, it could be argued that the different cognitive symptoms suggest separate disorders rather than different manifestations of the same disorder. Again, MDD is marked by thoughts of loss (high negative affect, low positive affect) whereas anxiety deals with fears (high negative affect, but no relation to positive affect). Furthermore, anxiety is marked by more physiological hyperarousal, whereas MDD is more cognitively-based and can lead to hypoarousal (e.g., fatigue, anhedonia).
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What is the evidence to support the bipolar/unipolar distinction? |
1. bipolar disorder is highly heritable, but this is not true for unipolar depression, suggesting a higher relation to genetics. Those with bipolar disorder are likely to be related to someone with unipolar depression, but the relationship is not true the other way around.
2. There are major gender differences in rates and manifestation of unipolar depression, but this is not the case for bipolar disorder. 3. Bipolar disorder arises earlier and is marked by more frequent episodes of shorter duration than unipolar depression, suggesting something more than just the same underlying issue with different manifestations. |
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How does this impact nosological issues involved with comorbidity between mood and anxiety disorders? |
This can make things complicated when trying to determine how depression and anxiety are related. There is certainly a lot of overlap between MDD and GAD, but what about bipolar depression? Are we going to make the case that GAD is the same as bipolar as well, even though we have already said that bipolar and unipolar depression are different? To further complicate matters, anxiety disorders are relatively common in folks who have bipolar disorder, so everything seems to overlap with one another while at the same time appearing to be distinct. If bipolar and unipolar depression are different from one another, and anxiety disorders are common in both, then it suggests the anxiety disorders are not the same as either and are instead something separate, and the depression in each may just put a person at risk for developing an anxiety disorder.
When looking at overlap of symptoms for different disorders, there is a lot of overlap between disorders, but they seem to group into two different groups. That is, MDD and other mood disorders overlap with one another more than the anxiety disorders relate to the mood disorders, while at the same time the anxiety disorders generally overlap and relate to one another more so than with the mood disorders. GAD seems to be the one possible exception, and it is still debatable, but it is likely best to keep it as separate since there is not yet enough evidence to merge it into MDD or the mood disorders. |
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Describe an etiological model of somatoform disorder. What factors combine to trigger and maintain symptoms? |
1. Likely begin with a person experiencing (at least from their perspective) actual physical symptoms (eg, headaches and epileptic seizures).
2. The person then becomes hypersensitive to them, which may then believe that there is something wrong with them (eg, the headaches may be due to a brain tumor). 3. Worrying about these symptoms, and being hypersensitive to them, can increase stress and induce the symptoms, further confirming their existence. 4. Additionally, the symptoms follow the person’s perception of what they should look like (e.g., what a seizure looks like), which will confirm for them that they have a certain illness (since it will be a perfect match to their mental schema of that illness). 5. These individuals may then seek medical care to treat the symptoms. Since doctors will not see anything wrong, but they are afraid of missing something, they will continue to test the person over and over. 6. This constant testing serves to further reinforce the person’s perception that the symptoms are related to a real problem. Additionally, doctors will almost always find minor things “wrong” within the body (such as benign growths) that will further reinforce the perceived symptoms. 7. The person may begin to associate some secondary benefits to the medical treatments. (eg, getting tests may allow paid time off of work, get them more attention from concerned friends and family). That is not to say that the person is at any point faking the symptoms, but the symptoms recur due to the reinforcements. |
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What are the positive symptoms of schizophrenia? |
Positive symptoms: psychotic behaviors not seen in generally healthy individuals. These symptoms often contribute to a person’s “loss of touch” with reality. They include the following:
1. Hallucinations: hearing (auditory), seeing (visual), smelling (olfactory), tasting (gustatory), and feeling (tactile) things that others cannot. Auditory hallucinations are most common among individuals with schizophrenia. These “voices” may talk to the individuals about his or her behavior, warn them of danger, or order the individual to engage in certain behaviors. 2. Delusions: false beliefs that are not apart of one’s culture and bizarre in nature. Beliefs are persistent even after there is proof that they are not true or logical. The delusions are sometimes characterized by paranoia (e.g., belief that others are trying to harm them in some way) 3. Disorganized behavior/speech: unusual ways or dysfunctional ways of thinking or speaking. Individuals may have difficulty organizing or connecting their thoughts logically. |
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What are the negative symptoms of schizophrenia? |
Negative symptoms: behaviors associated with disruptions to normal emotions and behaviors. They are sometimes harder to recognize as part of the schizophrenia and can be mistaken for depression and other conditions.
1. Anhedonia: the lack of ability to feel pleasure 2. Flat Affect: lack of emotional expression in face and speech (e.g., monotonous voice) 3. Positive & Negative Symptoms within Negative Symptoms Positive: Abnormal presence of anhedonia Negative: absence of symptoms |
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Describe the phases of schizophrenia. Phase 1 |
1. Prodromal: emergence of symptoms occurs during this phase (always occurring after puberty), somewhat due to hormonal changes
· 1 to 2 years before psychosis · Symptoms appear in isolation · Sharp decreases in school or work performance · Inappropriate or blunted affect (i.e., something good happens, no response) · Increase in anxiety symptoms (e.g., making decisions, concentrating) |
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Describe the phases of schizophrenia. Phase 2 |
2. Active (or acute): Symptoms appear psychotic: hallucinations, delusions, disorganized behavior
· Must rule out substance abuse during this phase to diagnose schizophrenia · At least three days to flush substances out of system |
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Describe the phases of schizophrenia. Phase 3 |
Residual: No active symptoms
· Negative symptoms may reappear · Lack of emotional expression, low energy, strange beliefs During a lifetime, an individual may have another active episode after being in the residual phase. Residual symptoms increase and the ability to function normally decrease after each active phase. |
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Describe the course of schizophrenia? |
Whether or not all schizophrenics in the prodromal phase or those “at risk” are likely to enter the residual phase over a lifetime is based on the presence number of risk factors and accompanied treatment.
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Describe the course of schizophrenia: Cannon et al. 2008 |
201 treatment seeking individuals at risk for schizophrenia (followed up each month). 35% converted to active psychosis
Predictors included: Genetic risk, recent deterioration of functioning, declaration of risk over time (hazard functioning: prodromal line is longer → probability lowers that one will get pass critical or “tipping point”) Means for intervention: antipsychotic medications Thus, in order to maintain stability of psychotic symptoms, the majority of individuals may function best on antipsychotic medications (possibly transitioning them to the residual phase). However, those not seeking treatment are more likely to engage in psychotic behaviors (active schizophrenia). Presumably, the stability of symptoms may be adjusted by antipsychotics in most individuals at-risk or in the prodromal phase of schizophrenia. |
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How has our conceptualization of the stability of symptoms over time changed from Emil Kraepelin’s initial proposal? |
This evidence is contrary to Emil Kraeplin’s initial proposal of dementia praecox, which was defined as a deterioration of the brain with worsening symptoms. Schizophrenia was considered to be a form of this disorder referred to as the “splitting of the mind” with a fluctuation of primary and secondary symptoms. The major difference in the conceptualization of schizophrenia now (based on Cannon et al. 2008) is that schizophrenia symptoms are treatable for most individuals and may get better over time with antipsychotic medications, which is contrary to the deteriorating condition Kraeplin describes.
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Describe some of the evidence that questions the cultural equivalence of the diagnosis of schizophrenia. |
Given the disproportionate amount of schizophrenia diagnoses among ethnic minorities globally, the cultural equivalence appears to be questionable. Individuals with a darker skin complexion have been found to be more likely to receive a schizophrenia diagnosis internationally.
1. In China, rural Chinese individuals would seek help for “demons” more often than urban Chinese, who are of a lighter skin complexion. 2. In Europe, migrant workers in Denmark, France, The Netherlands, and the United Kingdom have been found to have higher rates of schizophrenia. Those individuals with a darker skin complexion are 2.7 times more likely than the general population to receive a schizophrenia diagnoses 3. Also in Europe, blacks are 4.8 times more likely to receive a diagnosis 4. African Caribbeans in the UK are 9.1 times more likely to have a diagnosis of psychosis than other carribbeans in the UK |
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What implications does the cultural equivalence of schizophrenia have for DSM V? |
Reliability of clinicians to diagnose schizophrenia is severely questioned. As a result, more idiosyncratic expressions of schizophrenia may be a plausible explanation suggesting that there may be several developmental pathways leading to a diagnosis. Perhaps, DSM V should focus on developing a dimensional model of schizophrenia as symptoms may manifest differently. Perhaps also the DSM V should take into account the specificity and influence of cultural and contextual factors on predictors of schizophrenia, as well as symptoms of schizophrenia. The examination of the nature of the relations between culture, context, and predictors or symptoms may lead to more individualized diagnoses of schizophrenia, rather than taking a categorical approach.
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What are the major brain abnormalities related to symptoms of schizophrenia? |
1. Ventricles: areas with brain fluid are larger in people with schizophrenia
2. Sulci: wrinkles in brain are shallower/smaller 3. Left hemispheric torque: one side of brain is pushed up further 4. Hippocampus: volume is smaller in adults with schizophrenia (Only consistent finding, all others are not) |
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What evidence fails to support a brain atrophy hypothesis in the etiology of the disorder? |
1. Brain atrophy is not specific to schizophrenia. Other disorders, like dementia, show brain atrophy.
2. There are brain differences in untreated 1st episode psychotics, but little evidence that it deteriorates from that point. 3. No evidence of degeneration in brain scans, no evidence of cell damage (Glial cells deposit remnants in response to brain degeneration (reactive gliosis), don't see this) 4. Prospective longitudinal studies don’t consistently show deteriorated brains |
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Briefly summarize some of the research conducted on the prenatal influences of schizophrenia. |
Prenatal threats that increase the risk of schizophrenia:
1. Birth complications (especially hypoxia: cutoff of oxygen): Linear relationship between length of time cut from oxygen and increase risk of schizophrenia 2. Maternal stress prenatally: study from military invasions 3. Maternal viral infection: study from 1957 Helsinki flu epidemic (Depends on the trimester: Mom’s exposure to viral infection during 2nd trimester increases risk of schizophrenia, not 1st or 3rd) 4. Prenatal malnutrition: study from the Dutch Hunger Winter, end of WWII when a blockade to Holland cut off food supplies (depends on the trimester: malnutrition in the 1st trimester increased risk of schizophrenia, not 2nd or 3rd) |
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How could such early prenatal insults predict adult psychopathology re: schizophrenia? |
Suggests that there are different risk pathways that develop/affect neural processes, then describe the pathway model Patrick drew in class
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Explain the mechanisms through which expressed emotion relates to increased relapse of schizophrenia symptoms. Consider possible interactions and reciprocal effects.: Why EE attitudes manifest |
1. High EE attitudes in families with a member who suffers from mental disorder is norma. Mental disorders strain emotional and economic resources
2. D/S model can explain why some families have low EE and some have high EE Factors within relatives + stressors may = high EE 3. Diathesis: potential vulnerability factors in relatives that are associated with high EE Personality: less flexible, less tolerant, more internally based locus of control, makes more attributions to patient responsibility, more self critical High vulnerability are likely to have high EE even with low stressors, low vulnerability likely to need more stressors to manifest high EE 4. Possible stressors not related to patient’s sx since relation of EE & relapse found across different disorders Attribution model of EE would predict that criticisms related to behaviors relatives believe patient can change (psychomotor retardation, loss of interest vs. fever, hallucinations) and behaviors that violate family norms Therefore, criticisms related more to negative sx instead of positive sx Length of illness and how long relatives have been coping with illness 5. D/S approach shows that EE is not a trait or state but a “relational variable,” product of interaction between patient and relative characteristics 6. More research should look at how characteristics of tolerance, flexibility and locus of control develop in relatives. What factors influence these characteristics? |
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Explain the mechanisms through which expressed emotion relates to increased relapse of schizophrenia symptoms. Consider possible interactions and reciprocal effects.: Why relapse is associated with high EE |
1. High EE relatives as stressors
High EE relatives behave negatively (e.g. talk more & listen less, more criticisms) More negative reciprocity in interactions with high EE relatives High EE tend to be more controlling and except patients to have more control of their problems and problematic behavior 2. Behaviors of relatives may be due to patient’s behaviors Evidence for behavioral differences between patients in hi & low EE interactions 3. D/S explains situations when EE leads to relapse, need both vulnerability & stress |
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Explain the mechanisms through which expressed emotion relates to increased relapse of schizophrenia symptoms. Consider possible interactions and reciprocal effects.: EE and vulnerability to relapse |
Schizophrenia: many studies show patients with schizophrenia highly sensitive to stress & negative life events |
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