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Transcript
Anxiety Disorders
Dr Ali Kheradmand M.D.
Assistant Professor of Shahid
Beheshti Medical University
When does anxiety become a
disorder?


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Anxiety is a normal human response to objects,
situations or events that are threatening
Anxiety is different from fear due to its cognitive
component (i.e. fear of the future)
Anxiety can be helpful and adaptive (e.g. anxiety
about giving lectures!)
Anxiety becomes a disorder when out of
proportion or when it significantly interferes with
life.
Anxiety disorders…

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Highly treatable yet also resistant to
extinction
Often begins early in life
Reported more by women than men
Reported more in Western countries
Often comorbid both with other anxiety
diagnoses and with other disorder groups
(e.g. Mood disorders, psychoses)
General considerations for
anxiety disorders

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Often have an early onset- teens or early
twenties
Show 2:1 female predominance
Have a waxing and waning course over
lifetime
Similar to major depression and chronic
diseases such as diabetes in functional
impairment and decreased quality of life
There Are Two Types Of
Anxiety:

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
Anticipatory: feeling of distress occurring
while studying for or thinking about the exam.
Situational: feeling of distress occurring
while taking the exam.
It is important to be aware of when anxiety attacks you so that you
may use strategies in and out of the exam situation to manage the
anxiety.
How does test anxiety affect
you?
Test anxiety affects you in three ways:
Physiologically
Behaviorally
Psychologically
4. More considered
response based on
cortical processing
1. Thalamus
receives stimulus
and sends to both
amygdala and
cortex
Sensory Input
2. Amygdala
registers
danger
3. Amygdala
triggers fast
response
• Parts of the brain involved in fear response = thalamus, amygdala,
hypothalamus, which then instruct the endocrine glands and autonomic nerv.sys.
• Evolved fear module (pink) versus considered response (green) = “fight or flight”
versus “feel the fear and do it anyway (or do it differently)”!
8
Physiological reactions may
include:
- increased heartbeat
- tensed muscles
- perspiration
- dry mouth
Behavioral reactions may include:
- Inability to make decisions, act, or
express yourself.
- Difficulty reading and understanding
questions on an exam.
- Difficulty organizing your thoughts.
- Difficulty recalling or retrieving terms
and concepts.
Psychological reactions may
include:
- Feeling apprehensive or uneasy.
- Feeling upset.
- Having self-doubt or negative self-talk.
12
Primary versus Secondary
Anxiety
Anxiety may be due to one of the primary
anxiety disorders OR secondary to substance
abuse (Substance-Induced Anxiety Disorder),
a medical condition (Anxiety Disorder Due to
a General Medical Condition), another
psychiatric condition, or psychosocial
stressors (Adjustment Disorder with Anxiety)
The differential diagnosis of anxiety. Psychiatric and Medical disorders. Psychiatr Clin North
Am 1985 Mar;8(1):3-23
The Anxiety Disorders
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Specific Phobia
Social Phobia
Panic Disorder
without agoraphobia
Panic Disorder with
agoraphobia
ObsessiveCompulsive Disorder
Substance induced
Anxiety Disorder

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Post-traumatic Stress
Disorder
Generalized Anxiety
Disorder
Anxiety Disorder due
to a general medical
condition
Anxiety Disorder Not
otherwise specified
Epidemiology of anxiety
disorders
Damsa C. et al. Current status of brain imaging in anxiety disorders.
Curr Opin Psychiatry 2009;22:96-110
Specific Phobias

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Selective, persistent and out of proportion
Includes cognition that leads to behavioural
response, whether or not the threat is present
May be genetically, neurologically or
experientially based
Maintained through the processes of classical
and operant conditioning.
Specific Phobia

Epidemiology
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Etiology
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Up to 15% of general population
Onset early in life
Female:Male 2:1
Learning, contextual conditioning
Treatment

Systematic desensitization
Social Phobia

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A more pervasive, highly cognitive type of
phobia
Distinguishing feature is the fear of doing
something in front of others
May be situation or context (e.g. performance
versus interaction anxiety) specific
Fear of one’s own behaviour causing
negative attention from others
Social Phobia Epidemiology
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7% of general population
Age of onset teens; more common in women.
Stein found half of SAD patients had onset of
sx by age 13 and 90% by age 23.
Causes significant disability
Increased depressive disorders
Incidence of social anxiety disorders and the consistent risk for secondary depression in the first
three decades of life. Arch Gen Psychiatry 2007 Mar(4):221-232
What is going on in their
brains??

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Both groups ↑ medial prefrontal cortex
activity in response to intentional relative to
unintentional transgression.
SAD patients however showed a significant
response to the unintentional transgression.
SAD subjects also had significant increase
activity in the amygdala and insula bilaterally.
Blair K. Et al. Social Norm Processing in Adult Soical Phobia: Atypical Increased Ventromedial Frontal cortex
Responsiveness to Unintentional (Embarrasing) Trasgressions. Am J Psychiatry 2010;167:1526-1532
What is going on in their
brains??
Blair K. Et al. Social Norm Processing in Adult Soical Phobia: Atypical Increased Ventromedial Frontal cortex
Responsiveness to Unintentional (Embarrasing) Trasgressions. Am J Psychiatry 2010;167:1526-1532
Agoraphobia

Marked fear or anxiety for more than 6
months about two or more of the following 5
situations:

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Using public transportation
Being in open spaces
Being in enclosed spaces
Standing in line or being in a crowd
Being outside of the home alone
Agoraphobia

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The individual fears or avoids these situations
because escape might be difficult or help might
not be available
The agoraphobic situations almost always
provoke anxiety
Anxiety is out of proportion to the actual threat
posed by the situation
The agoraphobic situations are avoided or
endured with intense anxiety
The avoidance, fear or anxiety significantly
interferes with their routine or function
Prevalence

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2% of the population
Females to males:2:1
Mean onset is 17 years
30% of persons with agoraphobia have panic
attacks or panic disorder
Confers higher risk of other anxiety disorders,
depressive and substance-use disorders
Panic Disorder




Two major types: with or without agoraphobia
Consists of a pattern of recurring panic attacks
Emotional, physical, cognitive and behavioural
components
Main fear is of losing control (consequence = dying,
going crazy, embarrassment, not being able to get help)

The fear of having a panic attack becomes a
problem of itself, possibly leading to
agoraphobia (fear of open spaces, crowds etc. Any place where
escape or finding help is difficult or embarrassing) or other phobias
A Panic Attack is:
A discrete period of intense fear in which 4 of the following
Symptoms abruptly develop and peak within 10 minutes:
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Palpitations or rapid
heart rate
Sweating
Trembling or
shaking
Shortness of breath
Feeling of choking
Chest pain or
discomfort
Nausea


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Chills or heat
sensations
Paresthesias
Feeling dizzy or faint
Derealization or
depersonalization
Fear of losing
control or going
crazy
Fear of dying
Panic disorder epidemiology

2-3% of general population; 5-10% of primary
care patients ---Onset in teens or early 20’s

Female:male 2-3:1
Things to keep in mind


A panic attack ≠ panic
disorder
Panic disorder often
has a waxing and
waning course
Post Traumatic Stress
Disorder


Is it an anxiety disorder?
Main diagnostic criteria:






Witness or experience of an event that (a) involved
actual or threatened death or injury, and
Feelings of intense fear, horror, or helplessness
Person must relive the event in some way (e.g.
dreams, “flashbacks”, internal distress, physiological
reactions)
Avoidance (subconscious and/or conscious)
Hyperarousal or mood instability
Usually persisting for at least three months
Generalized Anxiety Disorder


Excessive worry more days than not for at
least 6 months about a number of events and
they find it difficult to control the worry.
3 or more of the following symptoms:


Restlessness or feeling keyed up or on edge,
easily fatigued, difficulty concentrating, irritability,
muscle tension, sleep disturbance
Causes significant distress or impairment
Generalized Anxiety Disorder
Epidemiology



4-7% of general
population
Median onset=30
years but large range
Female:Male 2:1
OCD Comorbidities



>70% have lifetime dx
of an anxiety disorder
such as PD, SAD,
GAD, phobia
>60% have lifetime dx
of a mood disorder
MDD being the most
common
Up to 30% have a
lifetime Tic disorder

12% of persons with
schizophrenia/
schizoaffective
disorder
Obsessive Compulsive
Disorder
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Classified as anxiety disorder, but with unique
presentation
Characterised by obsessions and compulsions (in
most cases)
Compulsions may be physical or mental
Types of presentation: contamination fear;
doubt/checking; magic thinking; symmetry; hoarding
Severity = frequency + capacity to resist +
interference with normal functioning
OCD Etiology
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Genetics
Serotonergic
dysfunction
Cortico-striatothalamo-cortical loop
AutoimmunePANDAS
Treatment
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40-60% treatment response
Serotonergic antidepressants
Behavior therapy
Adjunctive antipsychotics, psychosurgery
PANDAS – penicillin, plasmapharesis, IV
immunoglobulin
Functional imaging studies


Increased activity in the right caudate is
found in pts with OCD and Cognitive behavior
therapy reduces resting state glucose
metabolism or blood flow in the right caudate
in treatment responders.
Similar results have been obtained with
pharmacotherapy
Baxter L. et al. Caudate glucose metabolic rate changes with both drug and behavioral therapy for
obessive-compulsive disorder. Arch Gen Psych 1992;49:681-689
Anxiety Disorders
Possible Causes
•
Tourette’s syndrome is characterized by muscular
and vocal tics: facial grimaces, squatting, pacing,
twirling, barking, sniffing, coughing, grunting, or
repeating specific words (especially vulgarities).
•
Tourette’s Syndrome

a neurological disorder characterized by tics and
involuntary vocalizations and sometimes by compulsive
uttering of obscenities and repetition of the utterances of
others
37
Trauma- and Stressor-Related
Disorders
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Acute Stress Disorder
Adjustment Disorders
Posttraumatic Stress
Disorder
PTSD continued
Presence of 1 or more
intrusive sx after the
event

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Recurrent, involuntary
and intrusive memories of
event
Recurrent trauma-related
nightmares
Dissociative reactions
Intense physiologic
distress at cue exposure
Marked physiological
reactivity at cue
exposure
Persistent avoidance by 1
or both:


Avoidance of distressing
memories, thoughts or
feelings of the event(s)
Avoidance of external
reminders of that arouse
memories of event(s) e.g.
people, places, activities
Negative alterations in cognitions and
mood associated with the traumatic
event(s) as evidenced by 2 or more of
the following:
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Inability to remember an important aspect of the
traumatic event(s)
Persistent distorted cognitions about cause or
consequence of event that lead to blame of self or others
Persistent negative emotional state
Marked diminished interest
Feeling detached from others
Persistent inability to experience positive emotions
Marked alterations in arousal
and reactivity with 2 or more
of:
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Irritable behavior and and angry outbursts
Reckless or self-destructive behavior
Hypervigilance
Exaggerated startle response
Problems with concentration
Sleep disturbance
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Duration of disturbance is more than one
month AND causes significant impairment in
function
Specifiers:
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With dissociative sx (derealization or
depersonalization)
With delayed expression (don’t meet criteria until
>6 months after event)
PTSD Epidemiology
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7-9% of general population
60-80% of trauma victims
30% of combat veterans
50-80% of sexual assault victims
Increased risk in women, younger people
Risk increases with “dose” of trauma, lack of
social support, pre-existing psychiatric
disorder
Comorbidities
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Depression
Other anxiety disorders
Substance use disorders
Somatization
Dissociative disorders
Functional neuroimaging in
PTSD
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Increased amygdal activation is seen in
PTSD pts compared to controls
Hypoactivation of the medial prefrontal cortex
including the orbitofrontal cortex and anterior
cingulate cortex (area implicated in affect
regulation)
Francati V. et al. Functional Neuroimaging Studies in Posttraumatic Stress Disorder:Review of
Current methods and Findings. Depression and Anxiety 2007;24:202-218

Study found treatment of PTSD with
paroxetine resulted in increased anterior
cingulate cortex function
Fani N. et al. Increased neural response to trauma scripts in posttraumatic stress disorder
following paroxetine treatment: A pilot study. Neurosci Letters 2011;491:196-201
Acute Stress Disorder
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Similar exposure as in PTSD
Presence of >9 of 5 categories of intrusion,
negative mood, dissociation, avoidance, and
arousal related to the trauma.
Duration of disturbance is 3 days to 1 month
after trauma
Causes significant impairment
General treatment approaches

Pharmacotherapy
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Antidepresssants
Anxiolytics
Antipsychotics
Mood stabilizers
Psychotherapy- Cognitive Behavior Therapy
Crank up the serotonin

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Cornerstone of treatment for anxiety
disorders is increasing serotonin
Any of the SSRIs or SNRIs can be used
How to use them
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Start at ½ the usual dose used for
antidepressant benefit i.e citalopram at 10mg
rather than the usual 20mg
WARN THEM THEIR ANXIETY MAY GET
WORSE BEFORE IT GETS BETTER!!
May need to use an anxiolytic while initiating
and titrating the antidepressant
Other options
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Hydroxyzine- usually 50mg prn. Helpful for
some patients but has prominent
anticholinergic SEs
Buspirone-For GAD- 60mg daily
Propranolol-Effective for discrete social
phobia i.e. performance anxiety
Atypical antipsychotics at low doses for
augmentation in difficult to treat OCD pts
Anticonvulsants
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Valproic acid 500-750 mg bid (ending dose)
carbamazepine 200-600 mg bid (ending
dose)
Gabapentin 900-2700 mg daily in 3 divided
doses (ending dose)
Atypical antipsychotics at low doses for
augmentation in difficult to treat OCD pts
Mothers little helpers
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Benzodiazapines are very effective in reducing
anxiety sx however due to the risk of
dependence must use with caution
Depending on the patient may either use on a
prn basis or scheduled
DO NOT USE ALPRAZOLAM- talk about a
reinforcing drug!
For patients with a history of addiction or active
drug/ETOH abuse or dependence
benzodiazepines are not an option
Alternative Treatments
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Acupuncture
Aromatherapy
Breathing Exercises
Exercise
Meditation
Nutrition and Diet Therapy
Vitamins
Self Love