Anxiety Disorders

Anxiety can be adaptive

important for our survival
helps us to escape or avoid danger
medium amount can improve
performance on many tasks

Anxiety Disorders

occur when anxiety becomes

overwhelming and out of proportion to
circumstances

Focused Neuroanatomy
Amygdala- involved with processing of
emotionally salient stimuli
Medial prefrontal cortex (includes the
anterior cingulate cortex, the subcallosal
cortex and the medial frontal gyrus)involved in modulation of affect
Hippocampus- involved in memory
encoding and retrieval

Amygdalae perform primary

roles in the formation and
storage of memories
associated with emotional
events.
During fear, sensory stimuli
reach the basolateral
complexes of the amygdalae,
particularly the lateral nuclei,
where they form associations
with memories of the stimuli.
The amygdala, especially the
basolateral nuclei, are involved
in mediating the effects of
emotional arousal on the
strength of the memory for the
event

Hippocampus plays an important

role in the formation of
new memories about experienced
events.
The hippocampus contains high
levels of glucocorticoid receptors,
which make it more vulnerable to
long-term stress than most other
brain areas.
Stress-related steroids affect the
hippocampus in at least three
ways: first, by reducing the
excitability of some hippocampal
neurons; second, by inhibiting the
genesis of new neurons in the
dentate gyrus; third, by causing
atrophy of dendrites

Anxiety Disorders
Phobic anxiety disorder
Other anxiety disorder
Panic disorder
Obsessive-compulsive disorder
Posttraumatic stress disorder

Phobic anxiety Disorder

Classification (ICD 10)

Agoraphobia
Social Phobia
Specific Phobia
Other PAD
Unspecified PAD

Symptoms of Specific Phobias

fear of specific object or situation

avoidance of object or situation
recognition that fear in unreasonable

Subtypes of Specific Phobias

Blood-injury-injection
Situational: planes, elevators, enclosed
spaces
Natural environment: heights, storms, water
Animal: insects, animals

Types of Phobia
Simple Phobia
Social Phobia
Agora Phobia

Simple Phobia
Irrational fear of specific object or
stimulus.
Common in childhood
Gradually subside with age.

Most Common Phobias

snakes
heights
enclosed spaces
illness
death
storms
dentists
injury

Social Phobia
Irrational fear of performing activities in
the presence of other people.
The patient is afraid of his own actions
being viewed by others critically,
resulting in embarrassment.

Prevalence of Phobias
11%
more common among women than men

sex ratio is 4:1

Agora Phobia
Irrational fear of being in places away
from familiar setting (comfort zone)
As the agoraphobia increases in
severity there is gradual restriction in
day-to-day activities & patient will
become self-imprisoned at home.

Causes: Learning Factors

classical conditioning
direct experience with a dangerous or painful
situation (50%)
panic attack (false alarm--probably triggered by
stressful life events) in a particular situation

vicarious conditioning
observing someone else experiencing severe fear

direct information transmission

being told repeatedly about danger

Maintenance of Phobias and

Learning

fear response and avoidance behavior

are maintained through negative
reinforcement
avoidance behavior prevents habituation to
the feared stimulus
avoidance behavior results in a reduction
in anxiety (negative reinforcement)

Causes: Biological Factors

natural selection
we are biologically prepared to acquire fear
responses to certain types of stimuli

genetics
some phobias (blood-injury-injection) are
particularly heritable

autonomic lability
sympathetic nervous system is responsible for
fight-or-flight response
some individuals have sympathetic nervous
systems that are more easily triggered and slow to
turn off

Causes: Cognitive Factors

phobics are more likely than nonphobics to

believe that frightening events will occur in
the future
phobics pay selective attention to threat cues
research using Stroop task
must name color of ink word in which word is
printed
phobics take longer to name ink for threat-related
words

Causes: Cognitive Factors

(continued)

phobics are more likely to misinterpret

ambiguous or neutral situations as
threatening

Treatment of Phobias

Exposure-based exercises
confronting feared object or situation
important to prevent person from engaging
in avoidance behavior (which results in
negative reinforcement)
often called exposure with response
prevention

Panic Disorder

Recurrent panic attacks in unexpected

situations

Symptoms of Panic Attacks

rapid or irregular pulse

shortness of breath
chest pain
sweating
feeling detached from
oneself
(depersonalization)
feeling detached from
ones surroundings
(derealization)

nausea
faintness
dizziness
trembling
choking
fear of dying
fear of losing control,
going crazy

Panic Disorder

Can be with or without agoraphobia

cluster of fears about having a panic attack
in public
may lead to drastic restriction in activities,
even becoming housebound

Prevalence of Panic Disorder

3.5%
most also have agoraphobia

more common among women than men

2/3 of cases are women

Causes: Biological Factors

autonomic lability:
sympathetic nervous system that is more easily
triggered, oversensitive, over reactive

some people are more likely than others to

have an emergency alarm reaction when
confronted with stress
may also lead to misfiring of sympathetic
nervous system
example: heart starts beating more rapidly than
normal for no apparent reason

Causes: Learning Factors

Classical

conditioning:

external cues (situations) and internal

cues (increased heart rate) become
conditioned stimuli that elicit panic
response.

Causes: Cognitive Factors

people with panic disorder pay more attention

to physical symptoms
also show heightened anxiety sensitivity
Unusual body sensations scare me.
When I notice that my heart is beating rapidly, I
worry that I might have a heart attack.
It scares me when I feel faint.
It scares me when I feel shaky (trembling).

Causes: Cognitive Factors

(continued)

people who develop panic disorder are

more likely than others to interpret
normal physical sensations in a
catastrophic way

Causes: A Vicious Cycle

fear of panic attack leads to increased

autonomic (sympathetic) arousal
physical sensations associated with
sympathetic arousal are interpreted as
dangerous, as signs of an uncontrollable
catastrophe
this interpretation further raises the anxiety
level and sympathetic arousal
eventually, a full-blown panic attack occurs

Medical Treatment of Panic

Disorder

antidepressants are first drug choice

SSRIs: increase levels of serotonin
fluoxetine (Prozac)
paroxetine (Paxil)
sertraline (Zoloft)
Tricyclics: increase levels of serotonin and
norepinephrine
imipramine (Tofranil)
clomipramine (Anafranil)
take about 4 weeks to work, but are generally safe
and not addicting
SSRIs are currently drug of choice

Medical Treatment (continued)

Benzodiazepines are also used in many

cases
short-acting: alprazolam (Xanax)
long-acting: diazepam (Valium)

very effective, and work quickly

problems
can be addicting
long-acting benzodiazepines increase risk of car
accidents, especially during first week

Medical Treatment (continued)

biggest problem with medical

treatments
many people relapse when they stop
taking the drug

Psychological Treatment of Panic

Disorder
exposure + cognitive therapy
key elements

exposure to external fear cues

exposure to internal fear cues
cognitive restructuring

highly effective
80-100% are panic free after 12 sessions
follow-up studies indicate that they remain
better 2 years later

Psychological Treatment
(continued)

biggest problems with psychological

treatment
it takes time for improvement
some people are too anxious to even
consider exposure therapy

Should we combine treatments?

rationale: meds work more quickly, but

psychotherapy is important for
preventing relapse

A Study of Combined Treatment

Experimental conditions
Drug only
CBT only
Drug + CBT
Placebo
Placebo + CBT

Combined Treatment (continued)

3 mos. into tx
All active txs better than placebo
Drug alone slightly better than CBT alone

6 mos. after tx ended

conditions involving drug deteriorated
lowest relapse rate was among CBT alone

Obsessive-Compulsive Disorder
(OCD)

Obsessions
recurrent, intrusive thoughts or images
seem irrational and uncontrollable to the person
experiencing them
cause distress

Compulsions
repetitive behaviors or mental acts that person
feels driven to perform
aimed at reducing distress or preventing some
dreaded event
washing and checking are the most common
compulsions

Prevalence of OCD

3%
55-60% of patients are female

Causes: Biological Factors

particular brain circuit has been implicated

worries normally start in the orbitofrontal cortex
then go to the caudate nucleus which filters out
trivial worries and
passes on serious threats to the motor cortex,
which executes actions in response to threats

caudate nucleus isnt filtering properly

Causes: Learning Factors

compulsions result in reduction of

anxiety (negative reinforcement)
compulsive behavior is maintained through
negative reinforcement

Causes: Cognitive Factors

efforts to suppress thoughts tend to
increase frequency of obsessions
people with OCD tend to show thoughtaction fusion

example: thinking about having an affair is

the moral equivalent of actually having the
affair

Medical Treatment of OCD

antidepressant medications are most

common
SSRIs
clomipramine (Anafranil)

60% of patients benefit

relapse rate (after go off drug) is high
in rare cases, brain surgery may be
required

Psychological Treatment of OCD

exposure with response prevention

person is gradually and systematically
exposed to the feared thought or situation
promotes habituation to the feared stimulus
prevents negative reinforcement of
compulsive behavior

facilitates reality testing

effective

Should we combine treatments?

Largest study to date

Conditions
exposure with response prevention (ERP)
clomipramine
clomipramine + ERP

Results
ERP alone superior to drug alone
85% responded to ERP
no advantage to combined tx

Posttraumatic Stress Disorder

(PTSD)

Exposure to traumatic event

Reexperiencing of event through memories,
flashbacks, nightmares
Avoidance of stimuli associated with trauma
Symptoms of increased arousal
(hyperalertness, disturbed sleep, difficulty
concentrating)
Numbing of responsiveness (feelings of
detachment from others, blunted emotional
responses)

Prevalence of PTSD
prevalence among general population is
7.8%
prevalence among survivors of trauma
is 17.9%

victims of rape = 33%

victims of serious car accidents = 25%

Causes: Biological Factors

stress responses are controlled by the

Hypothalamic-Pituitary-Adrenal (HPA) axis
causes release of stress hormones (adrenalin,
cortisol), which prepare body to respond to
emergency

severe stressors may cause permanent

changes in the HPA axis
results in chronically elevated stress hormones
may underlie chronic anxiety and exaggerated
startle response

Causes: Biological Factors

(continued)

chronically elevated stress hormones

may damage hippocampus
hippocampus plays an important role in
learning and memory; gives memories
narrative coherence and a location in time
and space
may underlie tendency for traumatic
memories to not make sense; instead
they come back as nightmares and
flashbacks

Other Risk Factors

Prior to the traumatic
event
exposure to traumatic
events in childhood
early family instability
high levels of daily
stress
pre-existing mood or
anxiety disorder

The traumatic event itself

severity
predictability (e.g.,
hurricane vs.
earthquake)
man-made or
technological disasters
worse than natural
events
more severe initial
reactions associated
with higher risk of PTSD

Protective Factors

social support following exposure to

trauma reduces chances of developing
PTSD

Treatment of PTSD

Psychological
Exposure to traumatic event (imaginally)
Content of trauma and emotions
associated with it are worked through
systematically

Medical
antidepressant medications (SSRIs,
tricyclics)
benzodiazepines are rarely used

Generalized Anxiety Disorder

(GAD)

Worry:
excessive, about multiple issues, uncontrollable,
occurs more days than not

Physical sx:
muscle tension, difficulty sleeping, susceptibility to
fatigue

Psychological sx:
mental agitation, irritability, difficulty focusing
attention

Duration: 6 mos.

Prevalence of GAD

5%
2/3 of patients are female

Causes: Biological Factors

Genetic factors:
inherit tendency to be anxious

Autonomic restrictors:
show less responsiveness to stress on
most physiological measures (heart rate,
skin conductance, blood pressure) than
individuals with other anxiety disorders
exception is muscle tension

Causes: Psychological Factors

Individuals with GAD show higher than

normal sensitivity to threat
research using Stroop task

Perception of threat is unconscious

words werent on screen long enough for subjects
to be able to name words

EEG studies show activity in left frontal lobe:

individuals engage in frantic, intense thought
processes without accompanying images.

Absence of images prevents

adaptation/habituation to feared situation

Medical Treatment of GAD

Benzodiazepines:
Give some relief in short term: after 6 mos,
benefits are modest
Impair cognitive and motor fx
Produce physical and psychological
dependence
Best use is for short-term relief associated
with temporary stressor

Antidepressants

Psychological Treatment of GAD

Help people to focus on what is actually

threatening
Cognitive behavioral therapy:
evoke worrying process, confront anxietyprovoking images and thoughts head on

Goal is to promote habituation/adaptation to

feared situation
Short term: as effective as meds
Long term: may be more effective than meds