Psych 100 Lecture 11: Clinical Psychology - Diagnostics, Disorders & Treatments PDF

Psychology 100: Clinical Psychology  What is ‘Abnormal’? All fields of medicine must define what is normal and what is outside the range of normal Abnormal psychology includes states of mind and behavior that deviate both from 1) the statistical average and 2) from wha...

Psychology 100: Clinical Psychology  What is ‘Abnormal’? All fields of medicine must define what is normal and what is outside the range of normal Abnormal psychology includes states of mind and behavior that deviate both from 1) the statistical average and 2) from what mental health professionals consider to be ‘healthy’ psychological functioning Classifying a behavior or states of mind as ‘healthy’ or ‘unhealthy’ is arbitrary Personal distress or impairment “One Flew Over the in function must also be present! Cuckoo’s Nest” (1975 film)  Diagnosing Mental Disorders Clinical psychologists (Ph.D., Psy.D.) and psychiatrists (M.D.) are trained in the diagnosis and treatment of mental disorders The Diagnostic and Statistical Manual (DSM) of Mental Disorders is the guidebook for diagnosis – Now in its 5th Edition The DSM provides a way of classifying mental disorders A disorder is diagnosed only if symptoms deviate from the statistical average, Number of Diagnoses DSM-5 541 there is psychological dysfunction and DSM-4-TR DSM-4 (in 2013) there is personal distress or impaired DSM-3-R DSM-3 253 (in 1987) functioning in life DSM-2 DSM-1 128 (in 1952)  Depressive & Bipolar Disorders (Affective Disorders)  Unipolar Depression “Major Depressive Disorder (MDD)” Unipolar depression consists of unremitting depression or periods of depression without mania Affects ~8% of the U.S. population yearly, with a median onset of age 32 Affects women 2-3X more than men Dysthymia is a milder, more chronic version Ø “Pervasive Depressive Disorder”  Symptoms of Unipolar Depression Depression is associated with a number of psychological and physical symptoms, including: – 1) Depressed mood – 2) Loss of ability to experience pleasure – 3) Restlessness, irritability and/or anxiety – 4) Lack of energy and concentration – 5) Difficulty falling asleep or staying asleep – 6) Constipation, aches and pains – 7) Thoughts of death or suicide A diagnosis requires that several of these symptoms be experienced over time and significantly impact functioning  Bipolar Disorder Bipolar disorder is characterized by cyclical periods of unipolar depression and mania Manic episodes can last a few days to several months; depressive episodes typically lasts much longer Affects ~3% of the U.S. population yearly, with a median onset of age 25 Affects men and women in roughly equal numbers Cyclothymia is a milder version  Symptoms of Mania Mania can range from mild (“hypomania”) to severe and may be characterized by: – High energy – Overly good mood – Cognitive clarity – Little need for sleep – Feelings of power – Fast, erratic talking – Racing thoughts – Impatience – Irritability  Stress & Depression The Diathesis-Stress Model The diathesis-stress Genetic Childhood model proposes that Predisposition Adversity depression arises due to two factors: 1) a vulnerability to Vulnerability depression Few stressful Excessive stressful 2) a stressful life event access circumstances or to coping circumstances and lack of access to (or series of stressful resources if stressed coping resources events) that the Low probability High probability individual is ill- of depression of depression prepared to cope with This idea is also applied to other mental illnesses! Depression & Hippocampal Atrophy PARTICIPANTS PRONE TO DEPRESSION Sheline et al, 1996, Proc. Natl. Acad. Sci., Vol. 93 Volume (mm3) Hippocampal (Across Lifetime) Volume (mm3) Hippocampal CONTROLS “Low Signal Foci” (a.k.a. holes!) Hippocampus (no history of depression) participant with a history in the hippocampus of a of depression Age A negative correlation (inverse relationship) exists between lifetime depression & hippocampal volume  Anxiety & Trauma-Related Disorders  What is an Anxiety Disorder? A psychological disorder characterized by persistent expression of several, or all, of the following symptoms: – Tension and worry – Overactivity of the sympathetic nervous system – Expectation of an impending disaster – Hypervigilance & arousal – Irritability – Avoidance of social activities A diagnosis requires that several of these symptoms be experienced over time and significantly impact functioning  Fear vs. Anxiety ! ? ? ? Anxiety is a state of Fear is evoked by threats tension over threats that are actually occurring that may occur in the future  Classifying Anxiety Disorders The lifetime prevalence for anxiety disorders as a whole in adults is about 25%! There are many types of anxiety disorders in the DSM-5: – 1) Phobias – 2) Panic Disorder – 3) Social Anxiety Disorder – 4) Generalized Anxiety Disorder – 5) Separation Anxiety Disorder Anxiety is a core symptom of PTSD, but PTSD is classified separately in its own category!  Post-Traumatic Stress Disorder Post-traumatic stress disorder (PTSD) results from exposure to a situation of extreme danger and stress Symptoms include recurrent recollections of the traumatic event, feelings that the traumatic event is recurring (‘flashbacks’), and intense psychological distress (hyper-vigilance and arousal)  Causes of PTSD Not everyone who experiences a traumatic event (even a very bad one) develops PTSD – The most common reaction of adults exposed to traumatic events is resilience! PTSD is associated with the number of traumatic events an individual has been exposed to as well as other types of pre-existing anxiety disorders A history of early life stressful or adverse experiences is a major predictor of who will develop PTSD Do these stressful/adverse events alter the structure and function of emotion circuits in the brain in a long-term manner?  The Diathesis Stress Model & PTSD Genetic Childhood Predisposition Adversity Vulnerability Few traumatic events Excessive traumatic or access to coping events and lack of resources during or access to coping after trauma resources Low probability High probability of PTSD of PTSD Vulnerability + Traumatic Experience = Likely PTSD!  Hippocampal Volume in PTSD Patients 3.0 Adapted from Lindauer et al, 2004 Hippocampal Volume 2.8 w/ PTSD Patients 2.6 2.4 2.2 2.0 1.8 1.6 ‘Traumatized’ 1.4 Controls 1.2 Patients ‘Traumatized’ w/ PTSD Controls (no PTSD) Amygdala Reactivity in PTSD Patients Threat Face Neutral MaskFace Amygdala Activation Adapted from Rauch et al, 2000 30 msec 500 msec Less Active More Amygdala Active Controls PTSD Patients  Dysfunctional Emotion Regulation in PTSD Prefrontal cortex Amygdala Less active than normal More active than normal Hayes et al, 2012 Patients with PTSD exhibit decreased activity in the prefrontal cortex and increased amygdala activity to threat! A Dysfunctional Emotion Regulation Circuit in PTSD UNDERACTIVE X Prefrontal IN H IB I TO RY Cortex Amygdala T ORY X C IT A E Classical NT RY HYPERACTIVE TO EXC Systems TA IT A CI EX HYPERACTIVE TO RY HPA Axis SNS HYPERACTIVE HYPERACTIVE  Treatment: Pharmacological Approaches  Depression & The Monoamine Hypothesis Depression has been loosely linked to the monoamine neurotransmitters – Dopamine (DA), Norepinephrine (NE), Serotonin (5-HT) Reserpine, a drug used to treat high blood pressure, was reported in the 1950s to cause depression – Reserpine interferes with the storage of monoamines (DA, NE, 5-HT) in synaptic vesicles Iproniazid, a drug used to treat tuberculosis, can alleviate depression – Iproniazid is a monoamine oxidase (MAO) inhibitor, which prevents the breakdown of monoamines The ‘Monoamine Hypothesis’ Monoamine levels low DA, NE, = Depression or 5-HT Monoamine levels high DA, NE, Depression or 5-HT = Sound a little simplistic???  MAO Inhibitors as Antidepressants (The “First Antidepressant”) MAO Inhibitor Iproniazid blocks MAO, preventing dopamine breakdown X Dopamine Transporter (re-uptake DA More dopamine is pump) available in the synapse Dopamine Note that all monoamine neurotransmitters are broken down in this way, so MAO inhibitors are non-selective!  Modern Antidepressants Nearly all modern antidepressants target one or more of the monoamines (DA, NE, 5-HT) Modern antidepressants include: Tricyclic antidepressants (TCAs): Older-generation, non-selective inhibitors of the reuptake of DA, NE & 5-HT (e.g., Imipramine, Desipramine) Selective Serotonin Reuptake Inhibitors (SSRIs): Highly selective for the 5-HT system (e.g., Prozac, Zoloft, Paxil, Lexapro, Celexa) Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Target 5-HT & NE reuptake more-or-less equally (e.g., Effexor, Pristiq, Cymbalta) Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs): No affinity for the 5-HT system (e.g., Wellbutrin)  Serotonin Reuptake PRESYNAPTIC NEURON Neurotransmitters returned to Remains of Presynaptic synaptic vesicle neuron presynaptic axon terminal Serotonin Reuptake Pump Action REUPTAKE Potential Serotonin Synapse ION FLOW ION FLOW Postsynaptic neuron Closed! Closed! Closed! POSTSYNAPTIC NEURON  Prozac & Serotonin Reuptake Inhibition PRESYNAPTIC NEURON Presynaptic Serotonin returned neuron Remains of to presynaptic axon terminal synaptic vesicle Serotonin Reuptake Pump Action Potential (Blocked) REUPTAKE Sero tonin Synapse Postsynaptic neuron Larger, more ION FLOW ION FLOW ION FLOW ION FLOW ION FLOW prolonged postsynaptic effect! POSTSYNAPTIC NEURON  A ‘Chemical Imbalance’? It is TRUE that monoamine- enhancing drugs (e.g., basically all modern antidepressants) can alleviate depression But that doesn’t mean that depression is caused by an ‘imbalance’ in monoamine neurotransmitters in the brain – There’s very little evidence for that! Do antidepressant medications alleviate depression by some other mechanism?  Antidepressants: Acute vs. Chronic Treatment Most antidepressant medications typically take 2-6 weeks of chronic, daily use for depression symptoms to remit – their effects on neurotransmitter re-uptake are very fast (within 30 mins) Are these drugs alleviating depression in a more complex way than simply increasing neurotransmitter levels at the synapse? Studies in rodents have linked successful anti-depressant effects to increased hippocampal neurogenesis!  Chronic Treatment with Antidepressants Increases Hippocampal Neurogenesis Adapted from Malberg et al., 2000, J. Neuroscience Neural Progenitor 8K * 7K Newborn Neurons Cells (in the hippocampus) 6K Maturation Integration 5K The hippocampus is 4K one of just a few brain regions that 3K continues to add new 2K neurons into adulthood 1K Exposure to chronic stress 0 Placebo 1 5 14 28 impairs hippocampal neurogenesis! Days of Prozac Treatment  How Do Antidepressant Drugs Really Work? Depression and anxiety are almost certainly associated with stress-related circuit-level alterations in the brain that disrupt one’s ability to 1) regulate negative emotions and/or 2) experience pleasure and reward – e.g., impaired communication between prefrontal cortex and amygdala; impaired communication in reward- related circuits (e.g., nucleus accumbens) Antidepressant treatments (of all kinds) are believed to target these dysregulated circuits and induce plastic (e.g., structural) changes in the neurons within them, allowing normal circuit function to resume Prof’s Take: Neural circuits are the future of Psychiatry!  Drug Treatment for Anxiety & PTSD Benzodiazepines are very effective (indirect) agonists of the GABA receptor – e.g., Valium, Xanax, Klonopin, Ativan – Extremely effective at blocking anxiety, but their effects are not long-lasting – The therapeutic effect of benzodiazepines is likely due to increased inhibition in the amygdala – Dependence is a concern  Benzodiazepines & the GABA Receptor Benzodiazepines potentiate the effect of GABA, leading to increased permeability of chloride ions through GABA receptors and increased hyperpolarization NOTHING BOUND GABA BOUND GABA + BENZODIAZEPINE BOUND Benzodiazepine Benzodiazepine binding GABA GABA Benzodiazepine GABA binding site binding binding site binding site GABA Cl- Cl- site Cl- site binding Cl- Cl- Cl- site Cl- Cl- Cl- Cl- Cl- Cl- Cl- Cl- Cl- Cl- Channel Cl- - Cl- Cl- Cl- Cl- Cl- Cl Cl- closed!  Antidepressants for Anxiety Disorders Benzodiazepines are very effective for anxiety, but they are not desirable for long-term treatment SSRIs (and SNRIs) are also used for anxiety and, if they work, they can be used in long-term treatment Some anxiety disorders (e.g., panic, generalized anxiety, social anxiety) respond better to antidepressants than others Antidepressant Treatment & Amygdala Reactivity Scan #1 Fear Neutral Fear Neutral Scan #2 8 Weeks of Zoloft 40 msec 60 msec 40 msec 60 msec 0.6 Before Treatment to the Threatening Face % Change in Amygdala 0.5 Sheline et al, 2001, Biological Psychiatry SSRI After Treatment 0.4 0.3 0.2 0.1 0 -0.1 -0.2 Left Amygdala Right Amygdala Treatment: Psychotherapy  Psychoanalysis The assumption with all psychoanalytic approaches is that there is some underlying conflict, some root cause that gives rise to all of the symptoms of a Sigmund psychological disorder Freud These conflicts must be uncovered and dealt with during therapy Find the cause(s) and you treat the disorder!  Talking & Free Association For Freud, the root causes of a mental disorder were assumed to be hidden away ( “repressed”) in the unconscious mind and could be revealed by talking Free association is a technique in which a relaxed patient (verbally) reports all passing thoughts in their head without reservation The analyst’s job is to listen carefully for clues in the patient’s language – These clues are said to reveal fragments of long- forgotten/repressed wishes, fantasies, memories, etc  What Do We Like About Freud? The idea that we possess unconscious perceptual, emotional and cognitive processing that influences our behavior is appealing, and also, in that narrow sense, happens to be true! The idea that development is a critical time window that parental/caregiver influences can impact the rest of our lives is appealing, and also happens to be true! The patient-therapist interaction/ relationship is very appealing, and important!  Why Did Academic Psychology Leave Freud Behind? Psychodynamic theory is overly complex Its concepts and practical outcomes are largely untestable and unmeasurable – e.g., how do you study “repression”? The practice relies heavily on patient self-report and the ‘creative’ interpretation of those reports by the analyst – e.g., every person’s experience in analysis is unique It is time-consuming and expensive – e.g., it may last 5-10 years! 20 years? 30 years?  Cognitive-Behavioral Therapy (CBT) Developed by psychiatrist Aaron Beck in the 1960s Beck hypothesized that psychological disorders are caused and sustained by maladaptive thought and behavioral patterns – According to Beck, the ‘symptoms’ are the cause! Cognitive-behavioral therapy (CBT) uses the knowledge of cognitive psychology and associative learning theory to develop empirically-verified, targeted therapies to treat the symptoms If you treat the symptoms, you treat the disorder!  The Vicious Cycle of Maladaptive Thinking, Affect & Behavior Negative thinking drives Biased Distorted Thoughts further negative emotion (“I knew this would happen”; “I’m such a loser”; “What’s the use?”; “Nothing Negative emotions drive will ever work out for further negative thinking me”) “Rodney”  Belief Modification in CBT: Challenging Rumination & Worry The cognitive-behavioral Rumination Worry therapist must first I failed I’m not going identify maladaptive, that exam! to graduate! usually negative, thought patterns and behaviors Nobody will The therapist then I should have done better! ever hire me! attempts to train the patient to think about My parents their life differently Why me? will think I’m a loser! This process requires consistent practice!  CBT & the Brain? (HINT: It’s all about modifying circuits!) Anthes, Nature, 2014  Long-Term Benefits of CBT vs. Medication Patients in Remission (%) End of Treatment CBT Group Medication Group Holland et al, 2005  Mindfulness-Based Cognitive Therapy (MBCT) Mindfulness training combined with CBT Mindfulness-based cognitive therapists may have no interest in the patient’s self-report of problems – e.g., problems are a fact of life and are just part of the ‘clutter’ of our mind that is distracting us from appreciating what’s happening now! The goal of therapy is to train the patient to focus on the present (e.g., “What am I feeling right now? What am I thinking now? What am I experiencing now?”) The key is to learn to notice, in a non-judgmental way, what is happening in the present moment!  THE PAST! THE PRESENT! THE FUTURE! Rumination Worry I failed I’m not going that to graduate! exam! I should have I won’t done better! get a job! My parents Why me? will think I’m a loser! Learning to focus on the present can break this automatic loop of rumination and worry!  (optional) There Are Apps for That! www.headspace.com The other ‘future’ (that’s already here): Empirically- supported, affordable mobile mental health!  Behavior & Exposure Therapies Exposure-oriented therapies are based on theory and methods of associative learning (including extinction) Systematic desensitization involves repeated, gradual exposure to a fear- or anxiety- provoking thing or situation to reduce its emotional impact Vir tual reality therapy has become a tool for treatment of specific phobias and PTSD  Does Psychotherapy Work? For certain types of disorders (e.g., anxiety, depression, phobias)...the answer is YES! – CBT, in particular, can be highly effective Psychotherapy can identify environmental and cognitive triggers that evoke and sustain the symptoms of mental illness, particularly for depression and anxiety disorders Empirically-suppor ted treatments are relatively short, experimentally verified therapy techniques for the treatment of psychological disorders  Empirically-Supported Treatments A major goal of modern academic Clinical Psychology is to develop, and empirically test, novel treatments for psychological disorders and their symptoms. DOES. IT. WORK ???