Anxiety Disorders Dr Ali - PowerPoint Presentation

Slide1

Anxiety Disorders

Dr

Ali

Kheradmand

M.D.

Assistant Professor

of

Shahid

Beheshti

Medical UniversitySlide2

When does anxiety become a disorder?

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.Slide3

Anxiety disorders…

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)Slide4

General considerations for anxiety disorders

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 lifeSlide5

There Are Two Types Of Anxiety:

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.Slide6

Test anxiety affects you in three ways:

Physiologically

Behaviorally

Psychologically

How does test anxiety affect you?Slide7

Sensory Input

2. Amygdala registers danger

3. Amygdala triggers fast response

4. More considered response based on cortical processing

1. Thalamus receives stimulus and sends to both amygdala and cortex

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)”!Slide8

8Slide9

Physiological reactions may include:

- increased heartbeat

- tensed muscles

- perspiration

- dry mouthSlide10

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.

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Psychological reactions may include:

- Feeling apprehensive or uneasy.

- Feeling upset.

- Having self-doubt or negative self-talk

.Slide12

12Slide13

The differential diagnosis of anxiety. Psychiatric and Medical disorders.

Psychiatr

Clin

North Am 1985 Mar;8(1):3-23

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)Slide14

The Anxiety Disorders

Specific Phobia

Social Phobia

Panic Disorder without agoraphobia

Panic Disorder with agoraphobia

Obsessive-Compulsive Disorder

Substance induced Anxiety Disorder

Post-traumatic Stress Disorder

Generalized Anxiety Disorder

Anxiety Disorder due to a general medical condition

Anxiety Disorder Not otherwise specifiedSlide15

Epidemiology of anxiety disorders

Damsa C. et al. Current status of brain imaging in anxiety disorders. Curr Opin Psychiatry 2009;22:96-110Slide16

Specific Phobias

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.Slide17

Specific Phobia

Epidemiology

Up to 15% of general population

Onset early in life

Female:Male

2:1

Etiology

Learning, contextual conditioning

Treatment

Systematic desensitizationSlide18

Social Phobia

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 othersSlide19

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

Social Phobia Epidemiology

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 Slide20

What is going on in their brains??

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;167:1526-1532Slide21

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;167:1526-1532Slide22

Agoraphobia

Marked fear or anxiety for more than 6 months about two or more of the following 5 situations:

Using public transportation

Being in open spaces

Being in enclosed spaces

Standing in line or being in a crowd

Being outside of the home aloneSlide23

Agoraphobia

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 functionSlide24

Prevalence

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 disordersSlide25

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 phobiasSlide26

A Panic Attack is:

Palpitations or rapid heart rate

Sweating

Trembling or shaking

Shortness of breath

Feeling of choking

Chest pain or discomfort

Nausea

Chills or heat sensations

Paresthesias

Feeling dizzy or faint

Derealization or depersonalization

Fear of losing control or going crazy

Fear of dying

A discrete period of intense fear in which 4 of the following

Symptoms abruptly develop and peak within 10 minutes:Slide27

Panic disorder epidemiology

2-3% of general population; 5-10% of primary care patients ---Onset in teens or early 20

’

s

Female:male 2-3:1Slide28

Things to keep in mind

A panic attack ≠ panic disorder

Panic disorder often has a waxing and waning courseSlide29

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 monthsSlide30

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 impairmentSlide31

Generalized Anxiety Disorder Epidemiology

4-7% of general population

Median onset=30 years but large range

Female:Male

2:1 Slide32

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 disorderSlide33

Obsessive Compulsive Disorder

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 functioningSlide34

OCD Etiology

Genetics

Serotonergic dysfunction

Cortico-striato-thalamo-cortical loop

Autoimmune- PANDASSlide35

Treatment

40-60% treatment response

Serotonergic antidepressants

Behavior therapy

Adjunctive antipsychotics, psychosurgery

PANDAS – penicillin,

plasmapharesis

, IV immunoglobulinSlide36

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;49:681-689Slide37

Anxiety

Disorders

37

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 othersSlide38

Trauma- and Stressor-Related Disorders

Acute Stress Disorder

Adjustment Disorders

Posttraumatic Stress DisorderSlide39

PTSD continued

Presence of 1 or more intrusive

sx

after the event

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, activitiesSlide40

Negative alterations in cognitions and mood associated with the traumatic event(s) as evidenced by 2 or more of the following:

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 emotionsSlide41

Marked alterations in arousal and reactivity with 2 or more of:

Irritable behavior and and angry outbursts

Reckless or self-destructive behavior

Hypervigilance

Exaggerated startle response

Problems with concentration

Sleep disturbanceSlide42

Duration of disturbance is more than one month AND causes significant impairment in function

Specifiers:

With dissociative sx (derealization or depersonalization)

With delayed expression (don

’

t meet criteria until >6 months after event)Slide43

PTSD Epidemiology

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 disorderSlide44

Comorbidities

Depression

Other anxiety disorders

Substance use disorders

Somatization

Dissociative disorders Slide45

Functional neuroimaging in PTSD

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;24:202-218Slide46

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;491:196-201Slide47

Acute Stress Disorder

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 Slide48

General treatment approaches

Pharmacotherapy

Antidepresssants

Anxiolytics

Antipsychotics

Mood stabilizers

Psychotherapy- Cognitive Behavior TherapySlide49

Crank up the serotonin

Cornerstone of treatment for anxiety disorders is increasing serotonin

Any of the SSRIs or SNRIs can be usedSlide50

How to use them

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 antidepressantSlide51

Other options

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 ptsSlide52

Anticonvulsants

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 ptsSlide53

Mothers little helpers

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 optionSlide54

Alternative

Treatments

Acupuncture

Aromatherapy

Breathing Exercises

Exercise

Meditation

Nutrition and Diet Therapy

Vitamins

Self Love