Anxiety Disorders Flashcards
HPA activation - hypothalamic pituitary adrenal activation
Affects multiple brain regions
Affects every organ system in the body - blood pressure, clots, etc
Concepts related to HPA activation: Stress, Fear, Panic, Anxiety
Essential for survival
Stress
Response to perceived demands (problems)
A certain amount is healthy, but too much overwhelms the ability to deal with it
Objectively demonstrable problem
Outweigh coping abilities
Fear
Present-oriented
Response to actual danger
Surge in sympathetic nervous system (fight or flight response)
Strong urge to escape
Panic
Sudden rush of intense fear and physiological symptoms (fight or flight) - same thing as fear, but with no reason for it - excessive
False alarm
Anxiety
Future-oriented (apprehension)
Future threat
Physical tension
When does anxiety become a disorder?
Must be High Intensity High Frequency Excessive/unreasonable - over exaggerated threat perception (must be this to be disorder) Distress and/or impairment
Anxiety disorder is Ubiquitous
AD are present in all cultures
Prevalence/ life time prevalence varies
Anxiety Disorder cultural prevalence
Highest in US = 22%
europeans are more at risk than latinos, asians and africans
Canada = 6%
Research issues for culture
Definitions of culture, ethnic heritage are blurry
Differences between generations of immigrants
Difficult to group heritage groups
Prevalence of Anxt.Ds - general pop
ADs are the single largest mental health problem in North America
- 7% Lifetime prevalence (usually mildly imparing)
- 3% 12 month prevalence
Prevalence of Anxt.Ds - Patients in primary care settings
18% (even excluding specific phobias)
Non-cardiac chest pain: 40% have Panic Disorder
Focal epilepsy: 19% incidence of AD (especially PD)
Impairment of anxiety disorders
Disrupts school and work
>20% can’t work because of ADs
Social withdraw and interpersonal problems
Personal distress
Anxiety disorders are Chronic
OCD, Social phobia , GAD -more likely for these
Can be lifelong conditions that wax and wane depending on situational factors
Risk Factor for anxiety disorders
Depression intertwined with AD - they share many symptoms
More likely to have Substance abuse
Greater risk for PTSD in response to trauma
Anxiety disorders Under-treated
Most receive medication that doesn’t work long term
Only 20-30% receive evidence based psychological treatments or counseling - usually not covered by public health care.
Etiology of Anxiety disorders
Genetics Biochemical Brain Circuits Parenting styles Modeling/vicarious learning (parental anxiety) Peer influences Individual learning experiences
Genetic influences of anxiety disorder
People inherit a non-specific, generalized predisposition - prone to experience Negative affectivity - bad emotions (formerly “neuroticism”)
Overly active physiological response
Shared with depression
Evidence for genetic influence on Anxiety disorders
Evidence = family studies,
twin studies - 12-26% for MonoZygotic - Higher heritability for some phobias
Biochemical factors
Neurohormonal systems. example: People prone to anxiety have a Hyper-reactive HPA
Neurotransmitters - serotonin, underactive gaba, more sensitive to norepinephrine
Brain regions associated with anxiety
Brain regions associated with anxiety
Amygdala hyperactivity
Ventromedial prefrontal cortex (insufficient function?)
Hippocampus - memory and detection of stimuli
Hypothesizes links with AD
Abnormal amygdala responsivity = abnormal threat assessment
insufficient vmPFC function = Inability to recall extinction information (i.e. absence of aversive stimulus)
Abnormal hippocampal function= Reduced capacity to distinguish safe and dangerous cues, more fear, Cortisol changes
2.5% and 5% of children meet criteria for an anxiety disorder. May cause
- Family problems
- Bullying at school
- Other disorders later
The big 3 parenting behaviors
Over-protective, over-controlling parenting = anxiety worse
Critical - hostile parenting - risks for every internalizing disorders altogether
Neglectful parenting
Barlow’s Triple vulnerability Model (IMPORTANT)
ANXIETY
Genetic, physiological predisposition (biological) LEADS TO General psychological vulnerability (life events take the physiologically reactive person and gives them a sense of helplessness - the world is dangerous and there is nothing I can do. Lack of self-efficacy) LEADS TO specific psychological vulnerability (unique learning experiences, this leads to different anxiety disorders) LEADS TO Anxiety Disorder
DSM-5 Changes in anxiety disorder categories
They were all together DSM1 = neuroses, DSM4 - All anxiety - but separated bc of different patterns of brain activations
a. Anxiety disorders
b. Obsessive-compulsive disorder and related conditions
c. Trauma and stressor related disorders
DSM-5 anxiety disorders
Panic disorder Specific phobia Agoraphobia Social phobia Generalized Anxiety Disorder (GAD)
Panic Disorder
Diagnostic features
Recurrent, unexpected panic attacks (with insufficient reason for panic) which are Sudden, Intense and Peaks within minutes
Physical symptoms of a panic attack
palpitations, pounding heart, or accelerated heart rate; Shortness of breath, smothering; chest pain, feeling of choking, Dizzy, unsteady, lightheaded, or faint, Nausea or abdominal distress, Trembling or shaking, Sweating, Paresthesias (numbness or tingling sensations), Chills or hot flushes
Psychological symptoms of a panic attack
Derealization or depersonalization, Fear of losing control, going crazy or dying
Diagnosis of Panic Disorder
Anticipatory anxiety and Worry about the consequences of the attack (or i’m going crazy)
Significant behaviour change - Situational or avoidance of Internal sensations
Safety behaviors - e.g. carry benzodiazepines (does decrease anxiety), avoiding places with low O2
Subtypes of Panic Attacks
Cued (situationally bound) - in certain situations = always.
Situationally predisposed - predisposed for attack is certain situations = sometimes
Unexpected - Panic comes out of nowhere (required for diagnosis)
Limited symptom attacks - not PD - but still debilitating
Prevalence of panic attacks and PD
1 in 3 people experience a panic attack
3% Meet criteria for panic disorder
Biological challenge studies of Panic disorders to study the difference between people who have PA and those with PD
Manipulations that increase CO2 in the body. More CO2 has been shown to cause panic attacks more often in people with PD.
Biological theories of Panic disorder are about
Neurochemical disturbance - related to more sensitivity to CO2 - 30-40% genetically transmitted
e.g. suffocation false alarm theory (Klein) = more chemoreceptors = panic
Cognitive model of PD
Catastrophic misinterpretations of one’s physical sensations (Clark) → People interpret body changes as a threat, which leads to panic
If they are informed about it = less likely to panic
Panic attack trigger explanation - Barlow and Clark
Barlow and Clark - internal or external
Perceived threat Leads to Apprehension Which leads to Bodily sensations (anxiety) –> Catastrophic misinterpretations → fear of the bodily sensations (cognitive interpretation) Leads to panic attack
Treatment of Panic Disorder
CBT is first line treatment - Education → tell patients what is going on with them
Interoceptive (internal sensation) exposure (with professional)
In vivo exposure → Person does the exposure to these bodily sensations in daily life
Diagnosis of specific phobias
Marked and persistent fear that is excessive and unreasonable
Cued by the presence or anticipation of a specific object or situation
Types of phobias
Animal
Natural environment (like hydrophobia, acrophobia)
Blood-injury injection (has a physiological cause)
Situational (fear of elevators, planes and claustrophobia)
Other (coulrophobia, kinemortophobia - due to uncanny valley - biological explanation. Or trypophobia and more)
Prevalence of Phobias
General population: specific fears are common
6.7% of population meet diagnostic criteria
Genetic vulnerabilities for Phobias
Blood-injury-injection phobia - higher heritability
Biological Preparedness - Evolutionary influence
2-factor learning theory for specific phobias
Phobias develop through 2 step process
Step 1: Classical conditioning - development of fear response
Step 2: Operant conditioning - anxiety leads to anxiety reduction through avoidance
Problems with 2-factor learning theory for specific phobias
- Sometimes there is an Absence of conditioning event
- There are Individual differences in conditionability (some people are harder to condition to fears)
- Stimuli specificity - not every object is as easily conditioned
- Cognitive interpretations influence - people interpret situations differently
Rachman: 3 pathways - 3 ways of learning phobias
Direct conditioning - direct experience of aversive event
Vicarious conditioning - by watching
Informational transmission - self conditioning
Etiology of phobias
Interaction (Association) between innate vulnerability and learning experiences is the cause
Results in exaggerated threat perceptions - overestimated danger
Leads to avoidance and other safety behaviors
Safety behavior
major role in anxiety disorder development
Deliberate - Adopted to prevent negative outcome
Unnecessary
Animals also use safety behaviors
First line treatment for Phobias
In vivo Exposure
Graduated (step-wise) - little baby steps
use of imagined exposure
Phobia treatment - reconsolidation
reactivate the fear memory and store/reconsolidate the memory with fewer emotion connection. Relationships with fear decays.
Phobia treatment - extinction learning
Develop new memory store associated with feared stimulus.
Phobia treatment - Cognitive change
Reduce the selective attention to threat. Done through safety learning
Agoraphobia
Anxiety about being in places/situations where escape might be difficult or embarrassing or were help may not be available
Has to be in Multiple situations (versus simple phobia)
These situations are either avoided completely, entered with a safe person or endured with marked distress
One can have agoraphobia without panic and vice-versa
Commonly avoided situations in agoraphiobia
Buses, bridges, enclosed spaces, crowds, malls, movie theaters, standing in line-ups
Clinical picture of agoraphobia
Prevalence: 1.7%
Heritability: 61% - highest out of anxiety disorders (except for blood phobia)
Impairment: Safezone: housebound + Interpersonal problems (dependent on safe person)
Chronic course - only 10% remit without treatment
Treatment of Agoraphobia
CBT is first-line treatment
Education + In vivo exposure +Safety behavior fading - take safety away slowly +Relaxation and breathing instructions
Social Anxiety disorder (Social Phobia)
Marked or persistent fear of one or more social situations
Fears doing something humiliating or embarrassing and being negative evaluated
Subtype: performance only
Clinical picture
High prevalence in North America (8% CAD - 2% EU)
crystallizes in puberty, decrease with age. Onset 13yrs
more common in women
Taijin Kyofusho (Japan, Korea) - fear of offending people
Social and occupational impairment
Comorbidity with substance abuse and depression
Genetic contributors for social anxiety
Nonspecific vulnerability
Behavioral inhibition: Innate hypersensitivity to environmental change (high heart rate etc) and angry/disgusted faces (Jerome Kagan). Overprotective parents worsen this.
Cognitive-behavioral (Learning) contributors
Negative life events, self-beliefs and predictions leads to Selective attention which leads to Judgmental biases which leads to
Safety behaviors - may impair people by making them emotionally closed. They create the difficulties they are afraid of. This leads to negative predictions again. Cycle.
Treatment for social Anxiety
Serotonin reuptake inhibitors (SSRI) - high relapse if discontinued
CBT - lower relapse if discontinued
Treatment outcomes = Time course and relapse rates differs
