Lecture 13: Clinical Psychology

What is Abnormal:

All healthcare fields must define what is, “normal” and what lies outside the range of normal.

Abnormal Psychology:

The scientific study of unusual patterns of behavior, emotion, and thought, often aimed at understanding and treating mental health disorders.

What is the first part of abnormal psychology:

1) statistical average (e.g., how the, “average” person would behave,

What is the second part of abnormal psychology:

From mental health professionals consider to be, “healthy” psychological functioning.

Diagnostics

Are tool, procedures, and tests used by healthcare professionals to identify the presence, caused, and severity of diseases or medical conditions.

Clinical Psychologist:

(Ph.D., Psy.D.) and psychiatrist (M.D) are trained in the diagnostics and treatment of mental disorders.

The Diagnostic and Statistical Manual (DSM) of Mental Disorders is the guidebook of disorders:

The DSM provides a way of categorizing and classifying mental disorders.

How is a disorder diagnosed:

1) Symptoms deviate from the statistical average.

2) There is psychological dysfunction

3) There is personal distress or impaired functioning in life.

How many categories are there for Categorizing and Classifying Psychological Disorders?

There are eight categories.

Category:

-Substance-Use and Addictive Disorders

Examples (Subtypes):

-Alcohol Use Disorder

-Opiod Use Disorder

Symptoms:

Compulsive alcohol use; consistent impaired functioning at home, school, or work as a consequence of alcohol use; craving for alcohol; apparent loss of control over use.atC

Category:

-Schizophrenia and other Psychotic disorder

Examples (Substypes):

-Alcohol Use Disorder

-Opiod Use Disorder

Symptoms:

Compulsive alcohol use; consistent impaired functioning at home, school or work as a consequence of alcohol use; craving for alcohol; apparent loss of control over use.

Compulsive use of prescription opioid drugs; craving for opioid drugs; constant impaired functioning at home, school, or work as a consequence of use; apparent loss of control over time.

Category:

Depressive and Bipolar Disorder

Examples (Subtypes):

-Major Depression

-Bipolar Disorder

Symtoms:

Sad or listens mood; change in sleep, weight or appetite patterns; feelings of worthlessness and guilt; difficulty experiencing pleasure; fatigue, hopelessness, thoughts of death and suicide.

Swings between profound depression and highly engerized mood (mania). Mania can take the form of extreme elation, creativity, and grandiosity or anger and irritability; mania and depression are sometimes experienced simultaneously (mixed state)

Category:

Anxiety Disorders

Examples (subtypes):

-Generalized Anxiety Disorder

-Specific Phobia

Symptoms:

Chronic excessive worry and anxiety that is difficult to control, accompanied by factors such as restlessness or tension, fatigue, sleep disturbance, difficulty concentrating.

Excessive fear and anxiety experienced in the presence of a septic object or situation (e.g. spiders, snakes, blood, heights, air travel); intentional avoidance of the feared object or situation.

Category:

Obsessive-Compulsive Disorders

Examples (subtypes):

-Obsessive-Compulsive Disorder

-Hoarding Disorder

Symtoms:

Recurrent and persistent unwanted thoughts or mental images; combined with compulsive, repetitive, often ritualistic behaviors (e.g. hand-washing) that the person feels driven to perform and that take up a substantial amount of time and cause impairment or distress and dysfunction.

Difficulty and distress in discarding or parting with possessions (regardless of their lack of value); strong urge to save items, resulting in filling up and culturing living areas.

Category:

-Feeding and Eating Disorders

Examples (subtypes):

-Anorexia Nervosa

-Bulimia Nervosa

Symptoms:

-Refusal to maintain minimally normal body weight leading to abnormally low weigh; intense fear of gaining weight; disturbance in the perception of one’s body weight or shape.

Recurrent episodes of binge eating accompanied by inappropriate behavior (e.g. use of laxatives or induced vomiting) designed to keep the eating from resulting in weight gain.

Category:

Wake-Sleep-Disorders

Examples (subtypes):

-Primary Insonnia

-Narcolepsy

Symtoms:

-Chronic difficulty falling or staying asleep resulting in significant distress or impairment in important areas of life.

-Chronic, irresistible attacks of sleep at inappropriate times (e.g., sitting at the dinner table, walking alone on the street).

Category:

-Tramua and Stressor-Related Disorders

Examples (subtypes):

-Post-Traumatic Stress Disorder

Symtoms:

-After experiencing or witnessing an event that involves actual or threatened death or serious injury, one re-experinces the event in memory, nightmares, or flashbacks; avoids thoughts of the event or places in associated with the event; may have sleep or concentration problems and other symptoms.

Unipolar Depression:

Consists of a period of unremitting depression or periods of depression.

Unipolar Depression:

“Major Depressive Disorder (MDD)”

Consists of period od unremitting depression or periods of depression.

What is unipolar Depression not be due to:

Must not be due to substance use or normal grief (e.g, bereavement)

How much of the population does unipolar depression affects:

Affects 8-10% of the U.S population yearly, with a median onset of age 30-32.

Dysthymia:

Is a milder, more chronic version.

Symptoms of Unipolar Depression:

Depression is associated with a number of psychological and physical symptoms, including:

-Depressed mood (e.g., sadness)

-Restlessness, fatigue, irritability and/ or anxiety

-Sleep disturbances (either too much or too little)

-Difficulty thinking, concentrating or making decisions.

-Physical Symptoms (e.g., constipation, diarrhea, nausea, headaches, back and muscle pain, joint pain)

-Avoidance of social activities

-Loss of the ability to experience pleasure

-Thoughts of death or suicide

A diagnosis requires that several of these symptoms be experienced over time and significantly impact functioning.

Stress and Depression:

The “Diathesis-Stress Model”

The Diathesis-Stress model proposes that depression arises due to two factors.

What is the first reason of Stress and Depression according to The “Diathesis-Stress Model”:

1) A vulnerability to depression.

What is the first reason of Stress and Depression according to The “Diathesis-Stress Model”:

2) A stressful life event (or series of stressful events) that the individual is ill-prepared to cope with.

Add image of Diathesis-Stress Model:

What is Genetic Predisposition:

-A genetic predisposition means a person has an increased likelihood or developing a disorder because of their genes.

-It does not guarantee the disorder will happen.

-Environmental factors and life experiences also play a major role.

Genetic Predisposition and Depression:

-People with family members who have depression are more likely to develop:

-Major Depressive Disorder

-Persistent Depressive Disorder.

-Depression tends to run in families because certain genes’s may affect:

-Mood regulaition

-Brain chemistry

-Stress response

What is the Important Idea of Genetic Predisposition and Depression:

-Genes + environment + work together.

Examples of environmental triggers:

-Stress

-Tramua

-Loss

-Chronic illness

-Major life changes.

Example:

-Someone may inherit gene’s linked to depression, but appear after major stress or difficult experiences.

Key Point:

Genetic Predisposiiton= higher risk, not certainty.

Depression and Hippocampal A trophy:

A negative correlation exists between lifetime incidence of depression and hippocampus volume!

Anxiety Disorders: What is anxiety?

Fear:

Is evoked by threats that are actually occurring.

Anxiety Disorders: What is anxiety?

Anxiety:

Is a state of tension over threats that may occur in the future.

Classifying Anxiety Disorders:

The lifetime prevalence for anxiety disorders as a whole in adults is about 30-40%!

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!

Symtoms of Anxiety Disorder:

A psychological disorder characterized by persistent expression of several, or all, of the following symptoms:

-Feeling tense, nervous restless or irritable.

-Overactivity of the sympathetic nervous system (e.g., hyperventilation, increased heart rate, sweating)

-Sleep disturbances (either too much or too little)

-Excessive worrying and/or hyper vigilance

-Difficulty thinking, concentrating or making decisions

-Physcial symtoms (e.g, constipaition, diarrhea, nausea, headaches, back and muscle pain, and joint pain)

-Avoidance of social activates

A diagnosis requires that several of these symptoms be experienced over time and significantly impact functioning.

Post-Traumatic Stress Disorder: (PTSD):

Typically results from exposure to a situation of extreme danger and stress.

Post-Traumatic Stress Disorder: (PTSD):

Symptoms include recurrent recollections of the traumatic event is recurring (‘flashbacks’), and intense psychological distress (hyper-vilgance and arousual)

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 and individual has been exposed to as well as other types of pre-existing anxiety disorder:

-A history of early life adversity or stressful 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?

Dysfunctional Emotion Regulation in PTSD: A Meta-Anaysis

-Less active than normal

-More active than normal

Patients with PTSD exhibit decreased activity in the prefrontal cortex and inscresced amygdala activity to threats!

What is the Monamine Hypothesis?

The Monamine Hypothesis suggests that depression is linked to low levels or reduced activity of certain neurotransmitters in the brain called monamines.

The three major monamine neurotransmitters connected to depression are:

-Dopamine (DA)- Motivation, pleasure, reward.

-Norepinephrine (NE)- Alertness, energy, stress response.

-Serotonin (5-Ht): Mood, sleep, appetite, emotional regulation.

Low activity of these chemicals may contribute to symptoms of depression.

Evidence supporting the hypothesis:

1. Reseprine and Depression:

-In the 1960’s, doctors noticed that the drug Reserpine, used to treat high blood pressure, sometimes caused depression in patients.

-Reserpine works by interfering with the storage of monamines inside synaptic vesicles.

-The lowers level of dopamine, norepinephrine, and serotonin in the brain.

-Because depression appeared after monamine levels desceasced, researchers thought low monamines might cause depression.

2. Ipronaizaid and Relief of Depression:

-Another drug Ipronzaid, originally used for tuberculosis, was found to improve mood.

-Iproniazid is a monamine oxidase inhibitor (MAOI)

-MAOI’s prevent the enzyme monamine oxidase (MAO) from breaking down monamines.

-This increases level’s of serotonin, in dopamine, and norepinephrine in the brain.

-Since increasing monamines improved depression, this further supported the hypothesis.

Key Vocabulary:

Monamines:

Neurotransmitters involved in mood and emotional functioning

-Dopamine

-Norepinephrine

-Serotonin

Synaptic Vesicles:

-Small sacs inside neurons that store neurotransmitters before they are released into the synapse.

The Diagram explains how MOA inhibatators (Monamine Oxidase Inhibatators work as antidepressants):

Key Idea:

Normally, the enzyme MAO (Monomine Oxidase) breaks down neurotransmitters.

-Dopamine (DA)

-Norepinephrine (NE)

-Serotonin (5-HT)

In the synapse, neurotransmitters are usually:

-Dopamine (DA)

-Norepinephrine (NE)

-Serotonin (5-HT)

In the Synapse, Neurotransmitters are usually:

1. Released

2. Bind to receptors

3. Then either:

-Taken back up by transporters (retake plumps), or

-Broken down by enzymes.

What MAO Inhibitors Do:

Drug like Iponaized black the MAO enzyme.

Because MAO is blocked:

-Dopamine is not broken down as quickly.

-More dopamine stays in the synapse,

-Signaling between neurons increasces.

This can help improve mood in some people with depression.

Moa inhibitors do:

Why they’re called “non-selective”:

Moa enzymes break down all monamine neurotransmitters, not just dopamine.

Moa inhibatators:

Historical Importance:

Ipronazaid was one of the first antidepressants discovered, which help support the monamine hypothesis of depression.

Important Limitation:

-Moa inhibitors can interact dangerously with certain:

-foods (especially tyramine- rich foods like aged cheese)

-medications

-and stimulants

-Becausce of these risks, they are used less often today than newer antidepressants like SSRI’s.

Modern Antidepressants:

Nearly all modern antidepressants target one or more of the monamines (DA,NE,5-HT)

Tricyclic antidepressants (TCAs):

Older-generation, non-selective inhibitors of the reputake of DA, NE, & 5-HT.

(e.g., Imipramine, Desipramine

Selective Serotonin Reuptake Inhibitors (SSRI’s):

Highly selective for the 5-HT system (e.g, Prozac, Zoloft, Paxil, Lexapro, Celexa)

Serotonin-Norepinephrine Reputake Inhibitors:

(SNRIs): Target 5-HT and NE reputake more-or-less equally (e.g., Effexor, Pristiq, Cymbalta)

Norepinephrine-Dopamine Reputake Inhibitors:

(NDRIs): No affinity for the 5-HT system (e.g., Wellbutrin)

What is Serotonin Reputake:

After Serotonin (5-HT) is released into the Synapse and sends a signal between neurons, it is usually takin back into the original neuron by a Serotonin transporters (Reputake Pump)

This process is called reputake.

Why Serotonin Reputake matters:

-If Serotonin is removed too quickly:

-There is less serotonin left in the synaps.

-Which may reduce signaling related to mood.

SSRis (Selective Serotonin Reputake Inhibatators):

Many antidepressants work by blocking Serotonin Reputake.

Examples Include:

-Fluoxetine

-Sertaline

-Escitalopims

By blocking the transporter:

-More serotonin stays in the synapse,

-Serotonin signaling increases,

-Which can help improve depression symptoms for some people.

Basic Visual Idea:

Neuron releases Serotonin - Serotonin stays in the synapse longer- stronger signaling- Possible mood improvement.

What Benziaspines Do:

Benzodiazepines incresce the effects of GABA (gamma-aminobutric acid), the brains main inhibatory neurotransmitters.

GABA helps:

-Calm brain activity

-Reduces nervous system arousal

-And decrease anxiety

-Because benzopines strengthen GABA activity, they act as indirect agonists of a GABA receptor.

GABA Common Examples=

-Diazepam (valium)

-Arprazolam (Xanax)

-Conzepam (Klonopin)

-Lorazpam (Ativan)

Why they work for anxiety=

-These drugs increase inhabitation in areas such as the amygdala, which is heavily involved in=

-Fear

-Emotional Processing

-And Anxiety Responses

-More inhibition in the amygdala- less overactive fear signaling- reduced anxiety.

Benzodiazepines Advantages=

-Work very quickly

-Very effective for short-term anxiety relief.

-Can reduce panic symptoms rapidly.

Benzodiazepines Limitations/Risks:

-Effects are usually temporary

-The body can build tolerance

-Dependance and addiction can develop long-term use.

-Stopping suddenly may cause withdrawal symptoms.

What are Benzodiazepines usually recommend for:

-Short-term treatment

-Panic Attacks

-Or Temporary Severe Anxiety rather than long-term daily use.

Benzodiazpines and the GABA Receptor:

Benzodiazpines potentiate the effect of GABA, leading to increased permeability of chloride ions through GABA receptors and increased hyperpolarization.

Diagram: How Benzadispenzides affect the GABA receptor in the brain:

Step 1: Nothing Bound

-When nothing is attached to the GABA receptor=

-The chloride (CL-) channel stays closed,

-Very few chloride ions enter the neuron.

Result:

-The neuron can fire normally:

Diagram: How Benzadispenzides affect the GABA receptor in the brain:

Step 2: GABA Bound:

-When GABA binds into the receptor

-The Chloride (Cl-) channels stays closed,

-Very few chloride ions enter the neuron.

Result:

-The neurons can fire normally.

Hyperpolrazation means=

-The neuron becomes less likely to.

-Brain activity is slowed down,

-Calming effects occur.

Diagram: How Benzadispenzides affect the GABA receptor in the brain:

Step 3: GABA+ Benzodiazepine Bound:

-Benzodiazpines bind to a different site on the receptor than the GABA does.

-They do not open the channel themselves.

Instead they=

-Strengthen the GABA’s effect.

-Allow the chloride channel to open more often,

-Increase Cl- entry,

-Cause even greater hyperpolrization.

Result:

-Stronger inhibition of neurons,

-Reduced anxiety

-Sedation and Relaxation

Antidepressants for Anxiety Disorder:

-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.

A ‘Chemical Imbalance’?

-It is TRUE that monoamine-enhancing drugs (e.g., basically all modern antidepressants) can in some, but not all, cases alleviate depression and anxiety.

-But that doesn’t mean that depressive and anxiety disorders are caused by an ‘imbalance’ in monoamine neurotransmitters in the brain.

-There’s very little evidence for that!

How Do AntiDepressants Work?

Acute vs. Chronic Treatment

-Most antidepressant medications (typically) take 2-6 weeks (or more) of chronic, daily use for depression (or anxiety) symptoms to remit.

-In Constrast, the pharamacological effects of antidepressants medications on neurotransmitters reputake are very fast.

How do Effective Treatments for Depression and Anxiety Really Work?

Disorders such as depression and anxiety are almost certainly associated with stress-related circuit-level alterations in the brain that disrupts one’s ability to:

1) Regulate Negative Emotions and/or

2)Experience pleasure and reward

How do Effective Treatments for Depression and Anxiety Really Work?

Example:

There is likely impaired communication between prefrontal cortex and amygdala; impaired communication in reward-related circuits (e.g., nucleus accumbent), etc.

How do Effective Treatments for Depression and Anxiety Really Work?

Effective Treatments:

Effective Treatments (of all kinds, including both pharmaciological treatments) are believed to target these dysregulated circuits and induce plastic (e.g, structural) changes in the neurons within them, allowing nomal cicut function to resume.

Treatment and the Brain?

Both pharmacological treatments and all effective forms psychotherapy are ultimately thought to work by modifying circuits in the brain that restore one’s ability to effectively regulate emotions.

Psychoanalysis:

-The assumption with all psychodynamic approaches is that there is some underlying conflict, some root cause that gives rise to the symptoms of a psychological disorder.

-These conflicts and causes must be uncovered and dealt with during therapy.

(For the cause(s) and you treat the disorder!

Conscious

Thoughts, memories, feelings and desires that we aware in the present moment and that we can think and talk about rationally. (Ego Defense Mechanisms) (Rational, but not necessarily truthful)

Ego Defense Mechanisms

(Rational, but not necessarily truthful)

Talking and ‘Free Association’:

-For Freud, the root causes of 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 mind without reservation.

-The analyst’s job is 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 a strictly narrow sense, happens to be true!

-A critical time window that parental caregiver influences can impact the rest of our lives is appalling, and also happens to be true.

Why Did Academic Psychology Leave Freud Behind:

-Psychdynamic theory is overly complex.

-Its concepts and practical outcomes are largely untestable and unmemorable.

-The practice relies heavily on patient self-report and the ‘creative’ interpretation of those reports by the analysts.

Congnitive-Behavioral Therapy (CBT)

-Developed by psychiatrists 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-behvaioral therapy (CBT):

Uses the knowledge of cognitive pyschology and associative learning theory to develop empirically-verfied, targeted to treat the symptoms.

Belief Modification in CBT:

Challenging Rumination and Worry:

-The cognitive-behavioral therapists must first identify maladaptive, usually negative, thought patterns and behaviors.

-The therapists then attempts to train the patient to think about their life differently.

This process requires consistent practice.

Mindfulness-Based Cognitive Therapy (MBCT):

-Mindfulness training combined with CBT

-Mindfulness-based cognitive therapists may have no interest in the patients’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!

-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!

Behavior and Exposure Therapies:

-Exposure oriented therapies are based on theory and methods of associative learning.

Systematic desensitization:

Involves repeated, gradual exposure to a fear-or-anxiety provoking thing or situation to reduce its emotional impact.

Virtual reality therapy:

Is a kind of systematic desensitization that has become a tool for treatment of septic phobias and PTSD.

Client-Centered Therapy:

-Humanistic approach advocated by Carl Rogers.

-Patient is seen as a ‘client’ who is not “mentally ill”

-Therapists acts more like a ‘life coach’, allowing the client to reach their own solutions.

Unconditional Postive Regards:

Is a provided to encourage clients to make the right choices for themselves.

(A very different approach from that of Freuds)

Does Psychotherapy Work:

-For certain types of disorders (e.g, anxiety, depression, phobias the answer is yes)

-Psychotherapy can identify environmental and cognitive triggers that evoke and sustain the symptoms of mental illness, particularly for depression and anxiety disorders.

Empirically-supportted treatments:

Are relatively short, experimentally verified therapy teqniques 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 pyschological disorders and their symptoms.