Anxiety Disorders – an Outline



Anxiety Disorders – an Outline

Fears & Phobias

• Adaptive responses

• Excessive in nature

Fear: excessive fears

Phobia: subset of fears including avoidance fear, anxious anticipation, interferes significantly with daily routine, markedly distressed.

Social Phobia: 2 types: generalized versus nongeneralized.

Five subtypes: animal type; natural environment type; blood-injection type; situation type; “other” type.

Common fears: ontogenetic parade. These include: fear of separation; fear of unfamiliar adults; fear of animals, darkness, & imaginary creatures.

Adult fears: social fears; fears related to blood, illness, injury, or death; fear of animals; fears of environmental hazards.

Genetics: Mean heritability 40%. Environment or combination of both appears important.

Theories of Fear: 1. Two-factor Theory (Mowrer) & Pavlov, Watson & Rayner. Includes classical & operant conditioning. 2. Rachman (1976) which includes direct conditioning, modeling, & information/instructional transmission.

Prepared Fears (Seligman, 1970): 1. rapidly acquired 2. resistant to extinction 3. “noncognitive” 4. differentially associated with stimuli of evolutionary significance.

Research on preparedness theory: Cook & Mineka (1987, 1990); McNally (1987); Bandura

Behavioral & Cognitive Theories: 1. Neo-conditioning; 2. Neo-conditioning & emotional processing.

Anxiety Sensitivity: Reiss – AS is one of 3 fundamental fears. The others include illness/injury sensitivity & fear of negative evaluation.

Cognitive Model of social phobia: Clark & Wells (1995)

Panic Disorder with Agoraphobia

Issues with this disorder: controversy == 1. panic attacks and generalized anxiety are not qualitatively distinct forms of anxiety. 2. Agoraphobia is a major disability – why listed as secondary?

McNally (1994): Agoraphobia is a separate and distinct disorder from GAD

Are all panic attacks the same?

Lelliott & Bass (1990)

Ley (1992)

Subtypes of Panic & Agoraphobia

Other issues: cued versus uncued attacks?

Craske (1991)

Barlow (1994)

Nocturnal Panic: attacks occur during non-REM sleep & are different from night terrors.

Why does panic disorder progress to panic disorder with agoraphobia?

Two competing hypotheses: 1. spontaneous, unexpected panic should lead to extensive avoidance behavior b/c the individual has little idea of when/where the next attack will occur. 2. expected, situationally predisposed panic should result in phobic avoidance b/c the person believes there are identifiable situations that trigger the panic.

McNally (1994)

What predicts Agoraphobia?

Hallam (1978, 1983)

Craske & Barlow (1988)

Prevalence: 1.5-3.5%

Anxiety one year prevalence 17%

Social phobia appears more often than previously thought

Women 2x more likely = panic disorder / agoraphobia than men. Why?

Age of onset issues

The first panic attack

Comorbidity Issues: depression 24%; risk for suicide greater; Alcohol abuse 10-20%; alcohol population & panic (10-40%); comorbid hypochondriasis; social phobia 17%;

Klein: alcohol hypothesis

Contemporary Approaches to Panic Disorder:

1. Alarms, 2. Barlow (1988), 3. fear is evolutionary “hard wired” response 4. false alarms

Barlow==psychological vulnerability – poor control and predictability

Catastrophic misinterpretations: Clark (1986)

Anxiety Sensitivity

Neurotransmitter Dysregulation: Norepinephrine system; locus coeruleus; the role of serotonin.

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Neurotransmitters Primer ()

“A Neuron is a specialized nerve cell that receives, processes, and transmits information to other cells in the body. We have a fixed number of neurons, which means they do not regenerate. About 10,000 neurons die everyday, but since we start out with between ten and 100 billion (Hooper & Teresi, 1987), we only lose about 2% over our lifetime.

Information comes into the neuron through the Dendrites from other neurons. It then continues to the Cell Body – (soma) which is the main part of the neuron, which contains the nucleus and maintains the life sustaining functions of the neuron. The soma processes information and then passes it along the Axon. At the end of the axon are bulb-like structures called Terminal Buttons that pass the information on to glands, muscles, or other neurons.

 

 

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Anatomy of a Neuron

 

 

Information is carried by biochemical substances called neurotransmitters, which we will talk about in more detail shortly. The terminal buttons and the dendrites of other neurons do not touch, but instead pass the information containing neurotransmitters through a Synapse. Once the neurotransmitter leaves the axon, and passes through the synapse, it is caught on the dendrite by what are termed Receptor Sites.

Neurotransmitters have been studied quite a bit in relation to psychology and human behavior. What we have found is that several neurotransmitters play a role in the way we behave, learn, the way we feel, and sleep. And, some play a role in mental illnesses. The following are those neurotransmitters which play a significant role in our mental health.

Acetylcholine – involved in voluntary movement, learning, memory, and sleep

§ Too much acetylcholine is associated with depression, and too little in the hippocampus has been associated with dementia.

Dopamine – correlated with movement, attention, and learning

§ Too much dopamine has been associated with schizophrenia, and too little is associated with some forms of depression as well as the muscular rigidity and tremors found in Parkinson’s disease.

Norepinephrine – associated with eating, alertness

§ Too little norepinephrine has been associated with depression, while an excess has been associated with schizophrenia.

Epinephrine – involved in energy, and glucose metabolism

§ Too little epinephrine has been associated with depression.

Serotonin – plays a role in mood, sleep, appetite, and impulsive and aggressive behavior

§ Too little serotonin is associated with depression and some anxiety disorders, especially obsessive-compulsive disorder. Some antidepressant medications increase the availability of serotonin at the receptor sites.

GABA (Gamma-Amino Butyric Acid) – inhibits excitation and anxiety

§ Too little GABA is associated with anxiety and anxiety disorders. Some antianxiety medication increases GABA at the receptor sites.

Endorphins – involved in pain relief and feelings of pleasure and contentedness

Please note that these associations are merely correlations, and do not necessarily demonstrate any cause and effect relationship. We don’t know what other variables may be affecting both the neurotransmitter and the mental illness, and we don’t know if the change in the neurotransmitter causes the illness, or the illness causes the change in the neurotransmitter.”

 

Suffocation False Alarm Theory: Klein (1993)

Generalized Anxiety Disorder GAD == pervasive anxiety independently focused on minor events of everyday; excessive, frequency issues, uncontrollable.

Prevalence: 1.9 to 5.4%

2:1 female to male; 24 years, previously married, unemployed, homemaker

17% elderly men; 21.5 elderly women

Comorbidity: 82% significant impairment

75% co-occurring mental disorder

Age issues

Valid classification?

Later-onset GAD

What about pathological worry? GAD can be distinguished from other anxiety disorders on the basis of uncontrollable worry.

GAD associated symptoms: autonomic hyperactivity; motor tension; vigilance & scanning. GAD patients endorse symptoms of autonomic hyperactivity cluster, e.g. accelerated heart rate, shortness of breath).

Other measures of GAD associated symptoms.

Models of GAD: 1. vulnerability dimension 2. Model of pathological worry (Borkovec, 1994).

Why do some people develop this? Barlow

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Obsessive-compulsive disorder

Compulsions: repetitive behaviors (e.g. hand washing, checking) or mental acts (e.g. praying, couting)

**controversial: the person has to recognize that he disturbance is excessive & unreasonable (not children)

Obsessions: mental events (thoughts, images, impulses)

Current view: Obsessions == compulsions == neutralize the obsessions

What if the compulsive behavior is not evident? 2.1% of the cases

This might be important for treatment issues.

Changes to DSM-IV: Poor insight type

Epidemiology: prevalence 2.5%. An underestimate?

Study on college students = 10-15% of normal college students

Subclinical symptoms (e.g. intrusive thoughts, checking) precipitated by life stress (Parkinson & Rachman, 1981).

Gender: 50-60% female

Onset adolescence – mid 20s

Males 13-15; females 20-24

More insidious onset typical

Course: continuous

10-15% progressively deteriorating course

Comorbidity high: 50%: major depression, dysthymia, panic disorder, social phobia, specific phobia, common. Also personality disorders & tic disorders.

Obsessions: common thoughts of contamination; excessive doubting; concerns that tasks are not completed accurately; fear that accidentally caused harm to self or others; horrific or sexual images or impulses; need for symmetry or to have things in order; nonsensical thoughts or images.

Most common obsessions: contamination 45%; pathological doubting 42%; somatic 36%; need for symmetry 31%; aggressive or sexual obsessions 25%.

Common compulsions: washing & cleaning; checking; hoarding; reassurance seeking; adhering to certain rules and sequences.

Atypical compulsion: obsessional slowness

Mental compulsions: counting; internal repetition of material; forming corrective images to “neutralize” unacceptable ideas; cognitive attempts to suppressive obsessive thoughts/images

Patients are likely to have multiple compulsions & multiple obsessions.

Rasmussen & Eisen (1988) 80%

Most common: checking 63%; cleaning or washing 50%; counting 36%; assurance seeking 31%; symmetry or order 28%; hoarding 18%.

Model: compulsions cannot exist without obsessions. Foa & Kozak (1995) 90% / 1.7 % of sample

High rate of co-occurrence. Hudson & Pope (1990): GAD, specific phobias, somatoform disorders, habit disorders, tic disorders, delusional disorders, schizophrenia.

Family & Genetic Studies: Twin studies reveal genetic vulnerability in MZ vs. DZ twins

Early models: Mowrer (1960) two-factor theory. Not supported.

Cognitive Appraisal models, e.g. Salkovskis (1996)

Cognitive Deficit Models

Biological Models, e.g. neurochemical & neuroanatomical. Most popular = serotonin because of clomipramine or serotonergic drugs and their effects.

Structural: basal ganglia and orbito-frontal cortex.

**Multiple pathways for OCD: & add a learning piece.

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Orbito-frontal coretx

Post Traumatic Stress Disorder

One big issue: high-magnitude stressors vs. low-magnitude stressors. Is moral danger the key?

Does it matter if you are the recipient or agent of the trauma?

Prevalence: 7.8%

Women 2x more likely to develop the disorder 10.4% versus 5.0%.

Vietnam veterans lifetime rates 14.7% - 30% depending on the study.

Risk factors: male, extravert, neuroticism, less than college education, history childhood conduct disorder, family history of psychiatric disorder, black

#1 stressor = rape. Men 28.8% & women 29.2% develop PTSD after rape.

But.. only a small percentage of people develop PTSD.

Risk factors: female, neuroticism, lower social support, lower IQ, preexisting psychiatric illness (especially mood/anxiety), childhood physical abuse, childhood separation from parents; family history of mood/anxiety/substance abuse disorders; premilitary traumatic event; family instability.

What can protect you from developing PTSD? Basoglu et al (1994) = highly educated; politically committed; expected torture if captured; social & emotional support from family & friends; heroes upon release.

Retrospective Studies: peritraumatic dissociation predicts PTSD

Depersonalization predicts PTSD

Immediately following the trauma: acute symptoms

Most gradually improved

Chronic trauma produces lasting impairment in a significant minority of victims

40 year follow-up of WWII prisoners of war – chronic impairment in minority of victims.

Prevalence of delayed onset PTSD (Solomon) – 40% sought help; 33% worsening of symptoms; reemergence in future war time; other nonptsd disorders 4%.

Therapy: Some don’t get better even with therapy. Therapy can hasten remission 36 months versus 64 months. 1/3 remain symptomatic regardless of treatment.

Comorbidity: alcohol abuse; depression; GAD for men

Depression, GAD, alcohol abuse; panic disorder & dysthmia in women.

Higher rates of these co-occurring disorders: major depression; panic disorder; bipolar disorder; social phobia; alcohol abuse; 80% had 1 other disorder. 88% comorbidity in men; 79% in women.

Cognitive symptoms in PTSD: reexperiencing the raumas in forms of intrusive recollections, nightmares, flashbacks.

Coping Mechanism: disengage from the cues

Biological Symptoms: tonic autonomic arousal; physiologic reactivity; exaggerated startle response; Noradrenergic Dysregulation; sleep & nightmares (dreamlike/oneiric; movielike/eidetic).

Holocaust Survivors

Genetics: male Vietnam era MZ & DZ twin pairs.

Brain Imaging Studies: diminished hippocampal volume; risk factor for PTSD?

What predicts: lower intelligence predicts severity of PTSD symptoms even when you control for combat exposure.

Theoretical Models:

Inescapable shock (Seligman, 1976)

Two-factor Learning (Mowrer, 1939)

Kindling

Emotive Biasing

Information Processing

Is PTSD a normal stress response to an abnormal stressor?

Acute Stress disorder

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