Anxiety Disoders Flashcards
Generalised Anxiety disorder
- WHAT/ FIGS (prev, gender, race)
Excessive anxiety under most circumstances and worry about practically anything. Able to maintain relationships + life but on edge/restless/tired
- symptoms must last for 6+ months
FFs –>
a) Common in Western society (more than 6% will dev in their life)
b) 2:1 women
BRIEF aetiology of GAD -- Sociocultural perspective (2)
- Dangerous situations are likely to give rise to it
a) Katrina + earthquake in Hati – the residence who survived – anxiety disorders are twice as high (Derivois & Cenat, 2015)
b) Poverty – high poverty places there is higher crime rates, fewer educational & job opportunities and have greater rate of GAD (McLaughlin et al. 2012)
BUT
** not the whole picture as not everyone in poorer areas has it & people in wealthier areas can get it**
indepth aetiology
Cognitive perspective of GAD brief summary
- GAD caused by a maladaptive way of thinking; excessive worry is a cognitive symptom.
Metacognitive theory of GAD
WHO+WHAT
Wells’ model
Two types of worry
a) Type 1 worry: worrying about a non-cognitive process. Provokes an anxiety response. They try & cope with this arousal + decrease the arousal by creating positive beliefs about worry. THIS MAY DECREASE AROUSAL
b) Type 2 worry: worrying that your worrying is becoming uncontrollable === leads to ineffective strategies aimed at avoiding worrying (i.e. thought suppression,distraction)
***often unsuccessful –> can’t control their worry –> reinforce the belief that worrying is uncontrollable and dangerous
Meta cognitive theory GAD evaluation
FOR
1) Individuals with GAD experience more negative beliefs about worry and Type 2 worry relative to individuals without a diagnosis of an anxiety disorder
AGAINST
2) Similar levels of negative beliefs about worry and Type 2 worry as do those with OCD and panic disorder
3) most studies use MCQ + AnTI - two measures focus on perceived lack of control over worry, which are defining DSM-IV criteria of GAD. Thus, employment of these measures assert that an established diagnostic criterion for GAD discriminates individuals with GAD from those without GAD. Constructs of Type 2 worry and negative beliefs about worry need to be refined in these studies, or that different methodological approaches be employed
4) It doesn’t explain why many studies have shown an sustained physiological arousal
Contrast avoidance model
WHO + WHAT GAD
(Newmann + Llera, 2011)
- Rather than precluding negative emotional experiences, worry creates and prolongs a negative emotional state to prevent a sharp increase in negative emotions
- Based on findings that – compared to relaxation and neutral mood – worry led to greater negative emotions and physiological arousal and was later associated with lower subjective reactivity to negative emotional stimuli
- **Worry leads to sustained emotionality evidence – not reduces somatic activation **
Worry leads to sustained emotionality evidence – not reduces somatic activation
GAD
- Worry during a stressful period predicted higher anxiety and depression after the stress had ended (Segerstromet al. 2000)
- those with GAD report heightened emotional intensity and greater difficulty recovering from a negative mood state than non-anxious control participants (Mennin et al., 2005)
- Worry episodes heightened both concurrent and succeeding cardiac activity for 2 h following each worry episode (Pieper, Brosschot, van der Leeden, & Thayer, 2010)
MC vs Contrast avoidance model AREAS OF DIVERGENCE GAD
1) beliefs about worry fuel the maintenance of GAD. MC focuses on the role of negative beliefs (i.e. worrying about worrying),
CAM focuses on the fact persons with GAD and non-anxious controls demonstrate significant differences in their beliefs toward the utility of worry to control their emotional responses to external events (Type I worry)
2) the concept that Type I worry (i.e. the positive beliefs about worry) reduces somatic activation. BUT, substantial data suggest that worry is associated with sustained tonic somatic activation (and as a result it mutes acute reactivity to brief images
Biological perspective - GAD
- heredity
- GABA activity for/against
1) heredity - Researchers have found that biological relatives are more likely to have GAD than non-relatives (Shienle et al. 2011)
2) GABA - involved in feedback loop of fear; when GABA is released –> physical symptoms decrease (i.e. fear) BUT in GAD this GABA release = prohibited or prevented. Malfunction in this feedback system can cause fear and anxiety to go unchecked
well supported but has critics BC unsure if cause or consequence ALSO may be a circuit NOT just 1 neuroT*
BUT these brain circuits contain GABAgernic neurones
specific PHOBIAS
WHAT/FIGS (prev, gender, race)
what may phobia be also diagnosed with?
- Persistent + unreasonable fear of a particular object, activity or situation. People with a phobia become fearful if they even think about the object or situation they dread, but they usually remain comfortable as long as they avoid it or thoughts about it.
CAN BE SPEC OR GENERAL (agrophobia) - Almost 14% of people will develop a specific phobia at some point in their lives
- Women > men
- Race also influences phobia prevalence; black and Hispanic americans > white americans
- Not many in treatment
- agoraphobia
GAD anxiety circuit
in limbic system; amygdala –> hypothalamus –> muscles/brainstem –> reflexes; hyperactive in anxiety (Those with anxiety have a greater startle reflex)
Behavioural explanations of phobias (2)
+ one “but”
1) Modelling – observation + imitation. Person may observe that others are afraid of certain objects or events & develop fears of the same things
2) 2 events in proximity might come to be a trigger - classical conditioning
***leads to avoidance of X **
BUT to keep in mind:
phobias are highly resistant to extinction, whereas laboratory fear conditioning, unlike avoidance conditioning, extinguishes rapidly
what may phobia disorder become if there is “stimulus generalisation” ?
learned phobias may BECOME GAD
Social anxiety disorder
WHAT + FIGS (prev, gender, race)
- Severe, persistent and irrational anxiety about social or performance in which they may face scrutiny by others and possibly feel embarrassment
- Can be narrow i.e. about only public speaking OR broad such as a general fear of functioning poorly in front of others
- narrow: fear response + general: anxiety response
- ** either way = judgement as performing worse than everyone else***
1) 13% develop this disorder in their lives
2) women > men
3) minority > white
SAD culturally bound?
‘taijin kyofusho’ – fear of making OTHERS uncomfortable in Japan and Korea – may actually be fear of being evaluated negatively by others(?)
- Though there is evidence to suggest that different expressions of TKS overlap with SAD in other cultures, the rate of this disorder, and the meanings of the symptoms in those cultural contexts will greatly differ.
Cognitive explanation of SAD (leading exp)
- People with this disorder hold a group of social beliefs and expectations that consistently work against them: EG
a) They hold unrealistically high social standards thta they must achieve
b) See themselves as unattractive
c) Socially unskilled and inadequate
THUS avoid + fear social interaction; after a social situation –> will review + criticize how they “did”
- Cognitive theorists do not necessarily agree on why some have these cognitions and others do not – trait tendencies, genetic predispositions, child relationships, parental upbringing, biological tendencies
where do these thought patterns come from in SAD?
- temperament?
- shyness seems to be an important variable (this is heritable too)
where do these thought patterns come from in SAD?
- social experiences?
negative social experiences with peers may hasten the development of SAD or maintenance
where do these thought patterns come from in SAD?
- genetics
- family, twin, at risk studies
a) risk of developing SAD in a family with SAD was three times higher when compared with families with no SAD
b) twin studies: identical - 24% + frat 15%
Panic disorder
what + figs (prev, gender, race)
- Experiencing panic attacks unexpectedly and repeatedly
- May experience dysfunctional changes in their thinking and behaviour as a result of these attacks (i.e. plan their lives around the possibility of another attack)
- 5% will develop in their life
- women > men
- white > minority; experience of panic attack varies among cultures
what is panic disorder commonly linked with + why?
* often accompanied by agrophobia; said to set the stage for agrophobia. May become fearful of having panic attacks in busy places*
Biological explanation for panic disorder (2)
1) Norepinephrine activity is abnormal in people who suffer from panic attacks + antidepressants which help panic disorder affect norepinephrine activity
2) Norepinephrine is a part of a much bigger circuit - PANIC CIRCUIT (THIS IS DIFFERENT FROM ANXIETY CIRCUIT THUS THE TWO DIFFER)
a) anxiety used the lateral amygdala + prefrotnal cortex
b) panic pathway = central amygdala + periaqueductal grey
cognitive explanation of panic disorder
1
RECOGNISE THAT BIO ONLY EXPLAINS A BIT OF THE DEALIO
- Have a high degree of anxiety sensitivity – they focus on their bodily sensations much of the time + interpret them as threatening —-
- Also an intolerance to uncertainty?
1) People prone to panic disorder - overly sensitive to certain bodily reactions; they misinterpret them as medical catastrophe
EXAMPLE
i.e. people with panic disorder tend to ‘over breathe’ in stressful situs, abnormal breathing makes them think they are in danger of suffocation so they panic
Evidence surrounding cognitive theories of panic disorder
- Findings support the incremental, predictive
validity of panic-related interpretation biases - Said that interpretation bias is predictive of new onsets
of panic disorder (even when controlling for bodily sensations) (panic spec schema) - those who interpret things as threatening –> likely to dev PD later on
- those who have exp trauma = more likely to dev PD (congruent w this idea)
