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by: courtney caulfield

BBH432exam4studyguide.pdf BBH432

courtney caulfield
Penn State
GPA 3.3
Biobehavioral aspects of stress

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Biobehavioral aspects of stress
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This 21 page Study Guide was uploaded by courtney caulfield on Wednesday November 19, 2014. The Study Guide belongs to BBH432 at Pennsylvania State University taught by Dr.Shalev in Fall. Since its upload, it has received 399 views. For similar materials see Biobehavioral aspects of stress in Biobheavioral health at Pennsylvania State University.


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Date Created: 11/19/14
Courtney Caulfield BBH 432 Exam 4 Study Guide Let this list help focus your study This is not intended to be an exhaustive list See syllabus for the reading assignments to assist you with the material Oct 31 and Nov 3 Depression I amp ll 1 The etiology of mood disorders child maltreatment life events and social factors psychological and personality factors Influence of child abuse on adult depression Moderation by the Coritcotropin Releasing Hormone Receptor Gene These results suggest the possibility that heritable differences in CRHmediated neurotransmission exacerbate or dampen the effects of child abuse on the stress hormone system potentially modulating HPA axis sensitivity extrahypothalamic CRHergic circuits and risk for depressive symptoms in adulthood Life events Prospective research 4267 report a stressful life event in the year prior to depression onset romantic breakup loss of job death of loved one Social Factors interpersonal difficulties Lack of an intimate confiding relationship loneliness Behavior of depressed people often leads to rejection by others excessive reassurance seeking few positive facial expressions negative self diclosures slow speech and long silences Psychological Affect and Rumination Affect pattern of observable behavior associated with subjective feelings such as facial expression tone of voice and gestures Rumination the compulsively focused attention on the symptoms of one s distress and on its possible causes and consequences opposed to its solutions A lot similar to worry anxiety except worry focuses on the future and rumination focuses on bad feelings and experiences from the past Personality it has been suggested that certain personality characteristics predispose one to abnormal affect Neuroticism tendency to react with higher levels of negative affect predicts onset of depression 2 Know the different approaches for disorder classification DSM vs RDoC What are the critiques of the DSM diagnostic and statistical manual of mental disorders classification Disorders are classified with the purpose of science description allows communication providing homogenous groups to study enabling development of testable hypotheses DSM standard classification system of mental disorders published by the APA American Psychiatric Association Used by clinicians researchers psychiatric drug regulation agencies health insurance companies pharmaceutical companies legal system and policy makers Diagnostic classification depression or anxiety Diagnostic criteria symptoms duration behavior Descriptive test diagnostic features subtypes culture age gender features etc 5 different versions DSM I 1952 130 pages 106 mental disorders Mental disorders as reactions Definitions were simple brief paragraphs with prototypical descriptions DSM II 1968 134 pages 182 mental disorders Reaction terminology dropped and users were encouraged to record multiple psychiatric diagnoses in order of importance and associated physical conditions Practitioners using this were rarely in agreement when diagnosing patients with similar problems DSM Ill 1980 494 pages 265 diagnostic categories Descriptive and neutral atheoretical regarding etiology causes of disease Multiaxial classification system 5 axes Goal to introduce reliability Caveatlimitation medicalization of 2030 of the population who may not have had any serious mental problems Axis I clinical disorders substance abuse substance dependence mood disorders schizophrenzia Axis II personality disorders mental retardation borderline personality disorder antisocial Axis III general medical conditions cancer hypertension diabetes migraines chronic pain Axis IV psychosocial and environmental problems problems with primary support group occupational problems Axis V global assessment of functioning GAF GAF scale psychological social and occupational functioning DSM IV 1994 886 pages 297 mental disorders Inclusion of a clinical significance criterion required that symptoms cause clinically significant distress of impairment in social occupational or other important areas of functioning New disorders introduced acute stress disorder PTSD bipolar II disorder Asperger Others deleted cluttering passiveaggressive personality disorder DSM 5 2013 947 pages over 300 disorders 5 instead of V anticipates change DSM 5152 Reflects developmental lifespan New categories OCD and related disorders trauma and stressorrelated disorders Eliminated disorders sexual aversion disorder Combined disorders autism spectrum disorder New disorders social pragmatic communication isorder disruptive mood dysregualtion disorder premenstrual dysphoric disorder hoarding disorder excoriation skinpicking disorder binge eating disorder restless legs syndrome caffeine withdrawal cannabis withdrawal Critiques of DSM exhaustive nature leads some to complain everything is a disorder Although it is just a depressive episode such as bereavement grieving over a loved one s loss or dependent personality disorder not all of DSM diagnoses are treated as mental disorder on their own lack of biological validity antidepressants to treat grief The global pharmaceuticals market is worth 300 billion a year a figure expected to rise to 400 billion within three years No DSM5 task force or work group member is allowed to have more than 10000 of his or her annual income to be derived from industry sources nor are members allowed to hold stock or shares valued at more than 50000 in a pharmaceutical or device company David Kupfer MDChair of the DSM5 Task Force RDoc research domain criteria focuses on validity which DSM lacks NIMH natonal insititue of mental health directors says DSM is at best a dictionary for the field not a bible and NIMH will reorientate its research away from DSM categories RDoc is an attempt to create a new kind of taxonomy for mental disorders by bringing the power of modern research approaches in genetics neuroscience and behavioral science to the problem of mental illness Major domainsconstructs 0 Negative valence systems fear anxiety loss 0 Positive valence systems reward learning reward valuation 0 Cognitive systems attention perception working memory 0 Social processes attachment formation social communication perception of self and of others 0 Arousalmodulatory systems arousal circadian rhythms sleep and wakefulness each of the above domainsconstructs will be studies using different units of analysis aka 7 different classes of variables genes molecules cells neural circuits physiology behaviors and selfreports 3 Depression main symptoms and characteristics Who is most at risk to develop depression Depression 2quot leading cause of disability worldwide Main symptoms of depression depressed mood for at least 2 week period including most of the following Diminished interest in activities Change of more than 5 of body weight Insomnia or hypersomnia Psychomotor agitation Fatigue Feelings of worthlessness guilt Diminished ability to think or indecisiveness Recurrent thoughts of death or suicide Characteristics of Depression Episodic symptoms tend to dissipate over time Recurrent once depression occurs future episodes likely to occur average4 Subclinical sadness plus 3 other symptoms for 10 days significant impairments in functioning even though full diagnostic criteria are not met At risk women are more at risk than men 21 3x as common among the poor heritability from twin studies 4050 lifetime prevalence varies widely 3 in Japan to 17 in US 4 What is comorbidity and why it poses problem for research and diagnosis Comorbidity the presence of more than one disorder Someone with solely pure depression is rare patients usually have some degree of anxiety alcohol abuse ect This is problematic for the individuals as well as for research Depressive disorders are a public healthy priority and need costeffective interventions to reduce their burden 5 Biological bases of depression know the different approaches genes GXE neurobiological studies Genes due to the greater risk of major depression for females a hypothesis was formed that a dominant gene on the X chromosome might be involved failed to find this linkage with studies of DNA markers on the X chromosome Fathertoson inheritance common for both major depression and bipolar depression A megaanalysis of genomewide association studies for major depressive order Analyzed more than 12 million singlenucleotide polymorphisms SNPs in 18759 subjects half control and half MDD major depressive disorder cases NO SNPs achieved genomewide significance including analyses by sex recureent MDD recurrent earlyonset MDD age of onset and prepubertal onset MDD 1 lnfluence of life stress on depression moderation by a polymorphism in the 5HTT gene In a prospectivelongitudinal study of a representative birth cohort we tested why stressful experiences lead to depression in some people but not in others A functional polymorphism in the promoter region of the serotonin transporter 5HT T gene was found to moderate the influence of stressful life events on depression Individuals with one or two copies of the short allele of the 5HT T promoter polymorphism exhibited more depressive symptoms diagnosable depression and suicidality in relation to stressful life events than individuals homozygous for the long allele This epidemiological study thus provides evidence of a genebyenvironment interaction in which an individual39s response to environmental insults is moderated by his or her genetic makeup lnfluence of Child abuse on adult depression association study examining gene environment interactions between several genetic polymorphisms in the CRH type 1 receptor CRHR1 gene and measures of child abuse on adult depressive symptoms participation population 974 African American of low socioeconomic status high rates lifetime trauma These data support the corticotropinreleasing hormone hypothesis of depression and suggest that a gene x environment interaction is important for the expression of depressive symptoms in adults with CRHR1 risk or protective alleles who have a history of child abuse Charts childhood trauma questionarre CTQ and Beck Depression Inventory scores BDI yaxis child abuse xaxis Chart says that Child abuse interacts with the CRHR1 genotype to enhance risk for depression in adults Neurobiological Studies brain imaging structural studies that focus on of cells or connections in brain regions such as prefrontal cortex dorsolateral portion anterior cingulate dorsal portion hippocampus and amygdala functional activation studies focus on activity levels in brain regions depression shows diminished activity levels in prefrontal anterior cingulate and hippocampus and shows elevated activity in amygdala 6 Key brain regions involved in depression with particular emphasis on hippocampus Key brain regions involved in depression Orbital prefrontal cortex and ventromedial prefrontal cortex Dorsolateral prefrontal cortex wide connections to a variety of brain regions Primary function involves executive functioning such as planning cognitive flexibility and memory Amygdala Anterior cingulate involved with highlevel cognitive functions including inhibiton of inappropriate responses decision making and motivated behaviors Hippocampus post mortem hippocampus collected from 19 MDD and 21 control subjects In MDD the dentate gyrus and pyramidal neuron soma size is significantly decreased It is suggested that a significant reduction in neuropil in MDD may account for decreased hippocampal volume detected by neuroimaging In addition differential shrinkage of frozen sections of the hippocampus suggests differential water content in hippocampus in MDD 7 What is the monoamine hypothesis of depression What is the evidence for the involvement of norepinephrine serotonin and dopamine What are some of the limitations Monoamine hypothesis of depression depression results from the reduced activity of brain monoamines serotonin norepinephrine epinephrine dopamine antidepressant medications increase either norepinephrine or serotonin via blockade of monoamine reuptake Prozac selective serotonin reuptake inhibitor Evidence for involvement of norepinephrine in depression depressed patients have decreased norepinephrine and its metabolites in their cerebrospinal fluid and urine Genetic studies show that mice with genetically engineered functional enhancement of the norepinephrine system are protected from stressinduced depressionlike behaviors Therapeutic agents that specifically increase norepinephrine activity are effective antidepressants Evidence for involvement of serotonin in depression patients with major depression show deficient serotonin neurotransmission Serotonin uptakeinhibiting drugs prozac are most often used as antidepressants example of selective serotonin reuptake inhibitor SSRI serotonin is deacticiate in the synapse by reuptake into the presynaptic neuron but Prozac blocks this reuptake of serotonin thus increasing the activation of serotonin receptors Monoamine oxidase inhibitors MAOs long history of use for the treatment of depression bind to and inhibit MAOA preventing monoamine degradation This results in greater stores of monoamines available for release MAOA inhibitors are used in the treatment of depression People with depression have lower than normal levels of the monoamines and MAOA inhibitors restore the levels to within the normal range Evidence for the involvement of dopamine in depression hypofunction of the brain s dopaminergic system functions as rewarding pathway might result in loss of interest and lack of motivation core symptoms of major depression Limitations of monoamine hypothesis although antidepressants usually bring serotonin levels up to normal very quickly it takes 24 weeks before mood improves significantly therefore serotonin system dysfunction cannot be the sole cause of depression Intensive investigation has failed to find convincing evidence of a primary dysfunction of a specific monoamine system in depression Some antidepressants that have been known for a long time do not act through the monoamine system Experiments that cause depletion of monoamines do not cause depression in healthy people nor worsen the symptoms in depressed patients The hypothesis has been further oversimplified when presented to general public 8 What is the evidence for HPA axis dysregulation in depression How can you study it What is the difference in cortisol levels between depressed patients and controls I The stress system HPA axis is dysregulated in depression as evident by high levels of cortisol secretion of cortisol includes depressive symptoms and injecting cortisol in animals produces depressive symptoms hypercortisolism changes over time it is a processoriented perspective In acute depression there is an increased state of all hormones in the HPA axis but in chronic depression there is increased CRH and cortisol but low ACTH Postmortem enlarged adrenal glands Reduction in of CRH receptor binding sites Diminished hippocampal volume Functional tests blunted ACTH response to CRH administration due to downregulation of CRH receptors caused bt chronic CRH hypersecretion and impaired suppression of cortisol secretion after DEX administration DST test How do you study the HPA dysregulation evidence in depression DST dexamethasone suppression test blood test that assesses adrenal gland function by measuring how cortisol levels change in response to an injection of a steroid drug dexamethasone dex IS 25 times more potent than cortisol in its glucocorticoid effect and provides negative feedback to the pituitary to suppress ACTH secretion a patient takes a nighttime dose of 1 mg of DEX and the blood cortisol levels are measured in the morning if blood cortisol levels are relatively high test is positive and patient has an autonomous independent source of either cortisol or ACTH impaired suppression of cortisol secretion after DEX administration HPA axis related finding in depression DST in normal controls able to suppress cortisol after DEX administration DST in depressed patients unable to suppress cortisol after DEX administration In depression unable to suppress cortisol causes episodic hypersecretion of cortisol which affects somatic immune and cognitive function In contrast in PTSD the high level of cortisol suppression results in hypo secretion of cortisol 9 Know the main treatments for depression Interpersonal Psychotherapy IPT Cognitive Behavioral Therapy CBT Pharmacological treatments Pharmacogenetics Electroconvulsice therapy ECT Interpersonal Psychotherapy IPT short term psychodynamic therapy focus on current relationships Qgnitive Behavioral Therapy CBT monitor and identify automatic thoughts replace negative thoughts with more neutral or positive thoughts and behavioral activation activity assignments designed to increase positive experiences Pharmacological MAOI inhibitors isocarboxazis SSRI selective serotonin reuptake inhibitorprozac Pharmacogenetics specifically target HPA axis function CRH antagonists clinical trial using R121919 CRHR1 receptor antagonist a drug that blocks the receptor responses and shows improved symptoms in MDD patients Electroconvulsice therapy ECT reserved for severe depression with high risk of suicide depression with psychotic features treatment of non responders induce brain seizures by passing electrical current through the skull side effects are memory loss and headache Nov 5 amp Nov 7 Anxiety disorders I amp ll 1What is the definition of anxiety and why is it considered to play a normal adaptive function Anxiety a vague unpleasant emotion that is experienced in anticipation of some FUTURE misfortune Anxiety is a state of apprehension or uncertainty resulting from the anticipation of a realistic or imaginary threatening event or situation Anxiety may have emotional behavioral cognitive and physical components Anxiety plays a normal adaptive function Evolutionary viewpoint looks at traits in the context of natural selection and promotion of the species Primitive environment with much physical dangers anxiety had a protective function as a warning system and in helping escape Anxiety is a response to cues of potential danger avoidance aggression freezing Anxiety plays a normal adaptive function like preparedness we are more likely to become anxious in response to cues that represent ancient dangers snakes strangers storms blood Not likely to become anxious in response to flowers leaves shallow water or to more evolutionary recent dangers such as guns and cars Benefits of anxiety YerkesDodson aw performance improves as a function of anxiety up to a threshold beyond which there is a fall off in performance Increased arousal can help improve performance but only up to a certain point At the point when arousal becomes excessive performance diminishes 2 What is the relationship between stress and anxiety disorders Anxiety disorders are extremes of normal anxiety they occur when normal anxiety system becomes dysregulated excessive or inappropriate An anxiety disorder encompasses feelings of stress or anxiety and the behavioral efforts to cope with such feelings Relationship between stress and anxiety disorders dysregulation of the stress response contributes to the development of an anxiety disorder stress response excessive or prolonged unable to turn it off 3 Know some of the main symptoms and characteristics of anxiety disorders Symptoms of anxiety disorders Alterations in cognition worrying apprehension planning in response to anxiety focus on potential for harm Physical symptoms consistent with autonomic arousal sweating dry mouth rapid breathing increased blood pressure headache muscle tension Emotional Symptoms uneasiness edginess tension panic Behavioral symptoms avoidance behaviors compulsions Pathological anxiety causes significant distress in one s life and impairs ones ability to function normally Characteristics Of Anxiety Disorders Anxiety disorders are the SECOND most common mental disorder worldwide and FIRST in the US affectiong 40 million adults age 18 and older 18 of us population Lifetime prevalence of anxiety disorders 15 Anxiety disorders often present in early life If anxiety disorders are left untreated they tend to become chronic Comorbid disorders with anxiety depression and substance abuse Anxiety disorders exert a significant impact on ones quality of life 4 Etiology of anxiety disorders What are the main risk factors A complex set of risk factors cause anxiety disorders genetics neurobiological factors personality and life events Main risk factors of anxiety disorders are environmental Trauma from events such as abuse victimization death of a loved one Stress in relationship marriage friendship and divorce Stress at work school about finances from a natural disaster Lack of oxygen in high altitude areas 5 Know the major types of anxiety disorders No need to remember all the epidemiology details prevalence age of onset etc but you should understand the main features and differences between the major types of anxiety disorders GAD social phobia specific phobias including agoraphobia panic disorder and OCD Major Types of Anxiety Disorders 1Generalized Anxiety Disorder GAD Social Anxiety Disorder Social Phobia Specific Phobia Panic Disorder OCD PTSD U 39gt Generalized Anxiety Disorder GAD chronic anxiety uncontrolled excessive worry The person finds it difficult to control the worry and the anxiety and worry are associated with 3 of the following restlessness difficulty concentrating irritability muscle tension sleep disturbance fatigue Anxiety reported for at least 50 of the day and it is NOT focused on a particular element like specific phobia is The anxiety symptoms cause clinically significant distress or impairment in important areas of functioning international classification of diseases declares GAD when symptoms are present most days for weeks that include motor tension muscle tension twitching and shaking apprehension feeling on edge unable to cope poor concentration insomnia irritability and autonomic overactivity light headedness sweating tachycardia fast heart rate dry mouth epigastric discomfort Social Anxiety Disorder Social Phobia a persistent fear of social or performance situations in which the individual faces public scrutiny unfamiliar people Social phobia is when exposure to the feared situation almost always elicits anxiety The person with social phobia recognizes the fear as unreasonable or excessive The feared social exposure is associated with intense anxiety and distress blushing tremor butterflies Common anxiety provoking social situations are meeting new people interacting parties meetinfs speaking eating dealing with authority figures being assertive Specific Phobia persistent fear that is excessive unreasonable cued by the existence of of the anticipation of a specific object or situation snakes heights flying Exposure to phobia triggers anxiety immediately Recognition that the anxiety is excessive unreasonable Phobia is avoided or encountered with great distress common ones acrophobia heights algophobia pain astraphobia thunderstorms lightning 5 typed of specific phobias 1 animal 2 natural environment 3 bloodinjectioninjury 4sHua onal 5 other Agoraphobia fear of open spaces crowds or public places Fear of traveling by public transport fear that it may be difficult to get to a place of safety home People with agoraphobia avoid situations that don t have an immediately available exit risk factors stressful life events fam history domestic instability childhood fears overprotective mom autonomic symptoms tachycardia shortness of breath faintness sweating panic attacks are the marker of severity psychological fear dread behavioral avoidance to the extent that person becomes house bound cognitive I might have died Panic Disorder recurrent and unexpected panic attacks Panic disorders include anxiety about having a panic attack and consequences of the attack Panic attack a discrete period of fear discomfort in absence of real danger develops suddenly palpatations sensation that your heart is pounding sweating trembling shortness of breath etc OCD Obsessive compulsive disorder obsessions intrusive recurrent unwanted ideas and thoughts impulses that are hard to get rid of in spite of the fact that they produce great distress for the individual and compulsions repetitive behaviors actions or mental intended to decrease anxiety due to the obsessions Obsessions and compulsions significantly interfere with one s functioning and cause distress can have one or the other but rare usually have both together OCD has close links with depression 6 The cognitive theory of panic The cognitive theory of panic is the tendency to interpret a range of bodily sensations in a catastrophic fashion The cognitive theory of panic is selective attention to internal cues and avoidance of a panic attack increases the problem 7 Know the main treatments available for anxiety disorders in general Pharmacotherapy SSRls and MAOls SSRls used more for GAD than any other anxiety disorders Cognitive Behavior therapy Behavioral Therapy 8 Biological bases of anxiety disorders know the different approaches to study anxiety disorders Anxiety Disorders are studied by Genetic studies family twin adoption and molecular genetic studies Postmortem Neuropathological studies Neuroimaging Studies structural and functional neuroimaging Pharmacological studies in humans and animals which allows for investigation of neurotransmitter function Physiological Studies 9 Key brain regions involved in anxiety disorders Hippocampal atrophy Amygdala activation central structure in anxiety Activation of prefrontal cortex anterior cingulate orbitofrontal cortex 10 What are the main biological factors involved in anxiety disorders What is the role that each factor play norepinephrine GABA serotonin NPY To understand the biological factors involved in anxiety disorders you need to investigate the neural circuitry of the normal fear response and see where there is dysfunction and dysregulation Specifically NE and HPA axis and broder GABA serotonin neuropeptide Y NE norepinephrine dysfunction MAJOR role in the acute stress response and NE overactivity is implicated in anxiety disorders Studies have shown longterm alterations in NE system Continuous autonomic hyperarousal in response to traumatic stimuli HPA axis Dysfunction regulation of the HPA axis is by the amygdala and hippocampus which anxiety disorders cause hippocampal atrophy and amygdala activation A role for the CRH system in specific disorders panic and PTSD HPA axis abnormalities are more heterogeneous in anxiety disorders GABA dysfunction GABA is the main inhibitory neurotransmitter in the brain known to counterbalance the action of the excitatory NT glutamate abundance of GABA receptors found in cortex and limbic areas binding of GABA leads to increased inhibitory action A of drugs achieve their effect by modulating the GABA receptors In anxiety disorders there is a decrease in the inhibitory effects of GABA to counteract the increased activity of NE Serotonin anxiety disorders cause low inhibiton which results in less levels of serotonin SSRls block the reuptake of serotonin that helps treat anxiety disorders stressinduced activation of serotonin may produce anxiolytic inhibit anxiety 5HT1A recptors or anxiogenic causes anxiety 5HT2 Neuropeptide Y NPY inhibits the release of NE from sympathetic neurons that reduce anxiety and stress NPY knockout mice display anxiolyticlike phenotype Functional effects exhibited when injected into central nucleus of amygdaa produced Anxiolytic inhibit anxiety symptoms effects Nov 10 amp Nov 12 PostTraumatic Stress Disorder I amp ll Videos The memory pill httpwwwcbsnewscomvideosthememory pi 1 What other names were given to this disorder before the modern description of PTSD Shell shock physical shock of being close to exploding shells 2 What are the main differences between acute stress reactiondisorder and PTSD Main differences between acute stress reaction disorder and PTSD PTSD arises as a reaction to an acute stress reaction acute stress reaction is an overwhelming traumatic experience involving threat to life physical integrity of individual or a loved one car accident battle rape multiple bereavement grief due to loss terrorist attack natural disaster reaction includes daze disorientation mixed picture withdrawn or agitated autonomic symptoms onset within minutes resolved in 4872 hours Acute stress disorder is when symptoms last 2 days4 weeks following the event PTSD is when symptoms go beyond 4 weeks and have delayed onset ptsd came before acute stress disorder ptsd DSM Ill 1980 actue DSM IV 1994 PTSD does NOT trauma and trauma does NOT anything bad Misdiagnosis of PTSD is common no lab tests to detect it very treatable usually a comorbidity 3 PTSD criteria from the DSM what are the 3 categories 1 Reexperiencing intrusions at least 1 of the symptoms under this category to be diagnosed 2 Avoidance Numbing at least 3 of the symptoms under this category to be diagnosed 3 Hyperarousal symptoms at least 2 of the symptoms under this category to be diagnosed 4 What are the primary symptoms of PTSD Core symptom reliving the event flashbacks nightmares waking dreams Delayed or protracted response to the trauma Onset varies immediate or delayed Emotional numbness and detachment Avoidance of activities or situations that remind person of trauma 5 The prevalence of specific types of trauma and the probability to develop PTSD Victims of trauma related to physical and sexual assault face greatest risk of developing PTSD strength severity of stressor is what puts you at risk probability of PTSD RAPE men65 women 45 COMBAT men 40 Physical abuse women 50 men 20 Prevalence of trauma is very high among men less high among women 15 of those exposed to trauma will develop PTSD 6 What are the main outcomes for people with PTSD Main outcomes for people with PTSD they will have greater risks for other disorders 80 of people w PTSD will have another diagnosis depression substance abuse anxiety disorders Greater unemployment relationship problems health problems violence worse quality of life predictors of more outcome childhood trauma borderline or antisocial personality traits poor support network heavy alcohol intake 7 What is the role of the HPA axis in PTSD Roll of HPA axis stress response system in PTSD use the DXT test PTSD patients exhibit a high level of cortisol suppression resulting in decreased cortisol levels hyposecretion PTSD patients have high cortisol suppression in the DST test which means they have strong negative feedback inhibition of cortisol due to an increased sensitivity of glucocorticoid receptors which stress intolerance and emotional numbing Sensitization hyperarousal and reexperiencing 8 Key brain regions involved in PTSD Structural Functional Hippocampus amygdala Pre frontal cortex prefrontal cortex Anterior cingulate cortex 9 What is the role of the hippocampus in PTSD Know the seminal study on hippocampal volume and risk to develop PTSD What other evidence exist regarding changes in the brain and risk to develop PTSD after trauma Role of hippocampus in PTSD the hippocampus is necessary for declarative memory info facts and knowledge and involved in regulation of stress hormone responses negative feedback of HPA Exposure to stress can damage the hippocampus PTSD patients have poor memory Smaller hippocampus is a predisposing factor of PTSD Seminal study on Hippocampal volume and risk to develop PTSD Smaller hippocampal volume predicts pathological vulnerability to psychological trauma 40 male twin pairs 1 of each pair served in Vietnam war 1 did not 17 developed PTSD 23 did not Smaller hippocampal volume constitutes a preexisting vulnerability factor for pathological response to stress High PTSD severity is associated w lower hippocampus volume both in combatexposed twin and the noncombat exposed twin Other evidence that exists regarding changg in the brain and risk to develop PTSD after trauma MRI studies show PTSD is associated with a smaller hippocampus and cognitive impairment europsychological performance and IQ interaction between preinduction cognitive skills memory coding speed vocab and severity of combat exposure for PTSD including reexperiencing and arousal symptoms aka if you have poor hippocampal skills you are more likely to experience severe PTSD Prospective study Brain structural changes as vulnerability factors and acquired signs of postearthquake stress 42 nonPTSD subjects had brain imaging before the Great East Japan earthquake PTSD scores were negatively associated with the pre grey matter volume in the ACC processing of fear and anxiety and OFC orbitofrontal cortex ability to extint fear and anxiety of traumatic event 10 What did Dr Siver s study about PTSD after 911 tell us about coping styles that predict longer term risk of PTSD What is unique about this study Silver et Al psychological responses to 911 2700 people took survey online within 3 weeks after 911 was NOT restricted to people who were in NYC or DC on the day followup at 6 months A bigger trauma does not always more sever PTSD Diasthesisstress model diasthesis underlying vulnerabilitydisposition genetic psychological biological interacting with life events if negative life events then negative outcome if positive events positive outcome must study interaction between person and environment Coping styles at baseline predict longer term risk of PTSD 1 Giving up 68 2 Denial 33 3 Avoidance 31 Use of specific coping strategies shortly after an event is associated with symptoms over time Disengaging from coping efforts can signal the likelihood of psychological difficulties up to 6 months after a trauma What is unique about this study Shows that psychological effects of a major national trauma are not limited to those who experience it directly 11 What is the evidence that PTSD is influenced by the diathesis stress model 84 of the people in the survey who showed PTSD symptoms had pre 911 depression or anxiety 12 What are the results of the study by the WTC neighborhood study Who was most affected WTC neighborhood study 11000 highly exposed people of 911 studied 23 years later Results only 126 had full blown PTSD but many showed symptoms Injured most likely to develop PTSD followed by witnessed horror and last caught in a dust cloud Most affected older age female gender Hispanic low education and income divorce status 13 What therapies have been shown to be effective for PTSD Cognitive behavioral treatments are most effective for PTSD most evidence for cognitive processing therapy and prolonged exposure Medication also effective most evidence for antidepressants 14 Videos the memory pill What is it What stories are told What is the controversy What does the memory pill actually do in people vs mice 15 The p Factor What is the p factor and why is it important The p factor is the general psychopathology dimension Higher p scores more life impairment greater familiality worse developmental histories more compromised early life brain function P factors are important because they explain why it is challenging to find causes consequences biomarkers and treatments with specificity to individual mental disorders Nov 14 Guest lecture Cognitive Behavioral Therapy 1 What are the three factors influencing our core beliefs How can this be influenced by early experiences 3 factors influencing our core beliefs views about self views about the world views about other people 2 What is the basic model on which CBT is based The cognitive model the way we perceive situations influences how we feel emotionally Its not the situation but rather our thoughts about the situation that directly affects how we feel Distress inaccurate perspective which makes thoughts unrealistic CBT helps individuals to identify distressing thoughts and to evaluate how realistic they are the clients learn to change their distorted thinking this way Think more realistic feel better Emphasis of CBT solving problems and initiating behavioral change 3 What does the therapist focus on in CBT In CBT the therapist focuses on helping clients to overcome difficulties by changing their thinking behavior and emotional responses thoughts feelings behaviors Cognitive therapy beck and rational emotive behavioral theory ellis 4 What kind of skills is the therapist trying to develop Identifying distorted thinking Modifying beliefs Relating to others in different ways Changing behaviors Therapist focuses on building trust and rapport with clients from first contact and demonstrating empathy and collaboration Helping clients respond to inaccurate or unhelpful ideas psychoeducation When clients identify dysfunctional thinkinggtgtthey gain more adaptive and accurate perspectives examine the validity and usefulness of thoughts 5 Why is CBT helpful to PTSD PTSD clients perceive world as dangerous and symptoms they experience make their bodies feel unsafe they also have problems regulating their thought emotions behaviors and awareness so CBT Defines Trauma the body s response to an event CBT acknowledges that there may be experiences that cannot be controlled through rational thought flashbacks and dissociation of PTSD clients CBT focuses on the present moment with current thoughts and feelings being addressed in the hereandnow The therapist structures and guides the session w interventions that aim to alleviate symptoms and client vulnerability CBT helps clients challenge their beliefs and recognize when they start falling into maladaptive patterns Therapists help clients identify errors in thinking and replace them w realistic thoughts 6 What kind of cognitive distortions are common in PTSD Qgnitive distortions that are common in PTSD Fortune telling what if happens again Mindreading everybody thinks about me bc of what happened Emotional reasoning I feel j so now is going to happen Magnification the worst thing that could happen is if I have another flashback in public 7 What is the relationship between mind wandering and CBT How can mindfulness improve CBT Relationship between mind wandering and CBT mind wandering is linking to regions of the brain called Default Mode Network Experienced meditators who can identify mindwandering are able to deactivate the DMN thus the more this is practiced the more coherence and connectivity humans have between DMN and attentionfocused brain regions With practice CBT humans are able to train our minds to release distracting thoughts Mindfulness can improve CBT Intentionally paying attention with an open discerning attitude to the present moment and our immediate senses will help cognitive behavior therapy and decrease DMN 8 What types of symptoms alleviation are associated with CBT in PTSD Symptom Alleviation associated with CBT in PTSD Intrusive and upsetting memories thoughts or dreams about the trauma Avoidance of things situations or people that are trauma reminders Emotional numbing to physical reactions of hyperarousal Depression and anxiety Behavior problems Traumarelated shame Interpersonal trust Social Competence


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