Anxiety disorders in adults 2005

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ANXIETY DISORDERS IN CHILDREN & ADULTS

THEORY

DIAGNOSIS

TREATMENT

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Pharmacological response to medications designed to treat anxiety disorders is NOT evidence or proof of

ETIOLOGY.

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FEAR VERSUS ANXIETY

• FEAR

• OBJECTIVE

• PAST EXPERIENCE WITH STRESSOR

• KNOWN PROBALITY OF HARM

• ANXIETY

• SUBJECTIVE

• FUTURE ORIENTED

• UNKNOWN HOW ONE WILL BE HARMED

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NORMAL VERSUS ABNORMAL ANXIETY

• LEVEL OF ANXIETY

SOME LEVEL OF ANXIETY NECESSARY TO CREATE MOTIVATION

HIGH LEVELS OF ANXIETY RESULT IN INTERFERENCE WITH PERFORMANCE

HIGH LEVELS OF ANXIETY RESULT IN HIGH LEVEL OF COGNITIVE & PHYSIOLOGICAL AROUSAL

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• JUSTIFICATION

ANY LEVEL OF ANXIETY WOULD BE CONSIDERED ABNORMAL IF NO RATIONAL JUSTIFICATION EXISTS FOR THE SITUATION TO TRIGGER ANXIETY.

PERCEPTION OF THE EVENT AS THREATENING TO THE INDIVIDUAL’S SAFETY IS KEY.

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• INTERFERENCE IN FUNCTIONING

ANXIETY IS ABNORMAL IF IT CAUSES ANY

IMPAIRMENT IN FUNCTIONING IN ANY LIFE AREA:

(1) SOCIAL

(2) OCCUPATIONAL

(3) PHYSICAL

(4) RECREATIONAL

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PREVALENCE & INCIDENCEOF ANXIETY DISORDERS

• MOST COMMON MENTAL DISORDER IN UNITED STATES.

• 15%-TO-17% OF ADULT POPULATION SUFFER FROM 1 OR MORE ANXIETY DISORDERS.

23 MILLION HAVE ONE FORM OF THE 6 ANXIETY DISORDERS

• 5% -TO-10% OF SCHOOL AGE CHILDREN HAVE AN ANXIETY RELATED DISORDER.

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PREVALENCE & INCIDENCEOF ANXIETY DISORDERS

• 26% SUFFER FROM 2 OR MORE INDEPENDENT ANXIETY DISORDERS.

• 19% SUFFER FROM ONLY 1 ANXIETY DISORDER.

• 55% SUFFERED FROM MULTIPLE DISORDERS, ONE OF WHICH HELPED CAUSE THE OTHERS.

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ANXIETY DISORDERS

• Generalized Anxiety Disorder

• Panic Disorder

• Obsessive-Compulsive Disorder

• Post-Traumatic Stress Disorder

• Specific Phobia

• Social Phobia

• Agoraphobia w/o Panic Attacks

• Agoraphobia with Panic Attacks

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ANXIETY DISORDERS

• Anxiety Disorder Due to a General Medical Condition

• Substance Induced Anxiety Disorder

• Anxiety Disorder NOS

• Mixed Anxiety-Depressive Disorder

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GENERALIZED ANXIETY DISORDER

THEORY

DIAGNOSIS

TREATMENT

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Epidemiology of Generalized Anxiety Disorder

• One-year prevalence rate is approximately 3% of adults.

• Life-time prevalence rate approximately 5%.

• 25% of GAD patients present with comorbid condition:

Depression Panic Disorder Substance abuse Hypochondriasis Personality Disorder

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• Half of pts presenting for treatment report onset in childhood or adolescence.

• In children, Over-anxious Disorder of Childhood

• Gender ratio is approximately 2-to-1 females

• Course of disorder is CHRONIC but fluctuates & often WORSENS during periods of stress.

• familial association

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PSYCHOANALYTIC EXPLANATION OF GAD & PANIC DISORDERS

• INTERNAL CONFLICTS ARE SOURCE OF BOTH DISORDERS

• UNCONSCIOUS IMPULSES THREATEN EXPRESSION

• ANXIETY IS ALARM THAT DEFENSES ARE ABOUT TO BREAK DOWN.

• SINCE NO FOCUS FOR DEFENSE, ANXIETY SYMPTOMS ARE RESULT OF UNSUCCESSFUL DEFENSE AGAINST ANXIETY PROVOKING IMPULSES.

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COGNITIVE THEORY OF GENERALIZED ANXIETY DISORDER

Beck (1991) - People with GAD constantly make unrealistic assumptions that they are in imminent danger:

a. ANY STRANGE SITUATION SHOULD BE REGARDED AS DANGEROUS.

b. A SITUATION OR PERSON IS UNSAFE UNTIL PROVEN SAFE.

c. IT IS ALWAYS BEST TO ASSUME THE WORST.

d. MY SECURITY & SAFETY DEPEND ON ANTICIPATING & PREPARING MYSELF AT ALL TIMES FOR ANY POSSIBLE DANGER.

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GABA & ANXIETY DISORDERS

• Research points to a problem in feedback system can cause fear or anxiety to go unchecked (Lloyd, 1992).

• GABA is released to exert inhibitory action on excitatory activity of neurons.

• A second site on GABAA receptor binds with benzodiazepines.

• People with GAD may have ongoing problems with anxiety feedback system.

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GABA A Receptor with Binding Sites

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GABA & GENERALIZED ANXIETY DISORDER

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GABA & ANXIETY DISORDERS

• Brain supplies of GABA too low.

• May have too few GABAA receptors.

• GABA A receptors do not readily bind neurotransmitter.

• Brain may be releasing an excess of other

chemicals reducing GABA activity at receptor sites.

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ASSESSMENT OF GAD

SCREENING TOOLS

Anxiety Screening Questionnaire (15 items)

Primary Care Evaluation of Mental Disorders

(PRIME-MD)

Hamilton Anxiety & Depression Scale

Beck Anxiety Scale

Center for Epidemiological Studies Depression Scale

(CESD)

Hospital Anxiety & Depression Scale

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ASSESSMENT OF GAD

INTERVIEWING QUESTIONS:

“During the past 4 weeks, have you been bothered by feeling worried, tense, or anxious MOST of the time?”

“Are you frequently tense, irritable, and have trouble sleeping?”

If either answered YES, further investigation is warranted.

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TREATMENT OF GAD IN PRIMARY CARE

Treatment options – Most efficaciously treated by combination of CBT & Pharmacotherapy

Cognitive-Behavior Therapy

Reframing

Cognitive Restructuring

Identifying Anxiety Triggers

Cognitive Rehearsal

Stress-Inoculation

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Pharmacotherapy

SSRI• Paroxetine (Paxil) only FDA for GAD• Fluoxetine (Prozac)• Sertraline (Zoloft)• Citalopram (Celexa)• Fluvoxamine (Luvox)

• See Table 11.4 in Kaplan & Saddock for dosing.

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Pharmacotherapy – SSRI

• Advantages of SSRI

• Few side effects• Not addictive/dependence liability• Treats co-morbid depression• Once daily dosing• Low sedation effect

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Pharmacotherapy – SSRI

• Disadvantages of SSRI

• Patient does not experience symptom attentuation with single dose

• Several weeks to full therapeutic effects

• Gastrointestinal and Sexual side-effects common

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SNRI Venaflaxine Hydrochloride (Effexor XR)

• Approved by FDA

• Reduces symptoms of: anxious mood excessive motor tension restlessness insomnia irritablility poor concentration

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SNRI Venaflaxine Hydrochloride (Effexor XR)

• Common side effects: asthenia somnolence nausea tremor constipation abnormal ejaculation/orgasm

• Patient does not experience symptom attentuation with single dose

• Several weeks to full therapeutic effects.

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Nonbenzodiazepine agent – Buspirone (Buspar)

• It is a 5-HT1A 1A receptor partial agonist.

• More effective in reducing cognitive symptoms than somatic symptoms of GAD.

• Less addictive potential associated with its use.

• Indicated if patient has co-morbid substance use disorder.

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Nonbenzodiazepine agent – Buspirone (Buspar)

• Patients who had used benzodiazepines are not likely to respond to Buspirone.

• Lack or absence of anxiolytic effects (muscle relaxation & sense of well being) may be contributing factor.

• Effects take 2-to-3 weeks to become evident.

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Treatment of GAD

• BENZODIAZEPINES ALPRAZOLAM XANAX

CHLORDIAZEPOXIDE LIBRIUM

CLONAZEPAM KLONOPIN

CLORAZAPATE TRANZENE

DIAZEPAM VALIUM

LORAZEPAM ATIVAN

OXAZEPAM SERAX

PRAZEPAM CENTREX

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Pharmacotherapy – Benzodiazepines

• Advantages

• Therapeutic effect in single dose

• Time to full therapeutic effect in days.

• Anxiolytic effect of medications helps reduce somatic symptoms of GAD

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• Disddvantages

• Impaired alertness & motor performance• High addictive or dependence liability• Does not treat co-morbid depression• Requires several doses per day• High sedation effect• Memory impairment

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• Most common clinical mistake is to routinely continue treatment INDEFINITELY.

• Treatment may be minimum of 6 months-to-1 year so consideration of other medications who seem warranted.

• Start treatment with benzodiazepine & buspirone & taper off benzodiazepine when buspirone reaches maximum effect ( 2-to-3 weeks).

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PANIC DISORDER

THEORY

DIAGNOSIS

TREATMENT

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Epidemiology of Panic Disorder

• One-year prevalence rate is approximately 1.5% of adults.

• Life-time prevalence rate approximately 3.5%.

• Panic Disorder patients present with comorbid condition:

Major Depression GAD

Substance abuse OCD

Specific Phobia Agoraphobia

Social Phobia PTSD

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• Typically onset between adolescence & mid-30’s.

• Females 3X more likely to have PD with agoraphobia• Males 2X more likely to have PD W/O agoraphobia

• Course of disorder is CHRONIC but waxing & waning.

• 1st degree biological relatives are 8 times more likely to develop panic disorder.

• If onset before age 20, 20 times more likely

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NOREPINEPHERINE & PANIC DISORDERS

• Research has focused upon abnormal norepinepherine activity in locus coeruleus.

• Function of locus coeruleus is to send messages to amygdala (limbic system) that is known to trigger emotional reactions.

• Studies have indicated that locus coerulus is involved in activating certain behaviors such as increased vigilance.

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• Over-activity in nordrenergic system has been linked to panic disorder.

• Stimulation of locus coerulus in both animal & human studies trigger panic symptoms.

• Noradrenergic over-activity may be result of fewer GABAA receptor sites and lower GABA levels in occipital cortex of panic disorder patients. (Malizia, 1998; Goddard, 2001)

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• Anti-depressant drugs act to restore appropriate norepinepherine activity in locus coerulus & helps to reduce symptoms of disorder.

• 80% will experience some significant improvement.

• 40% reach full recovery or improve markedly; 20% show NO improvement.

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LOCUS COERULUS & PANIC DISORDER

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ASSESSMENT OF PANIC DISORDER

SCREENING TOOLS

Anxiety Screening Questionnaire (15 items)

Primary Care Evaluation of Mental Disorders

(PRIME-MD)

Hamilton Anxiety & Depression Scale

Beck Anxiety Scale

Center for Epidemiological Studies Depression Scale

(CESD)

Hospital Anxiety & Depression Scale

Panic Disorder Self-Test (www.adaa.org)

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Cognitive Behavior Therapy

Stress-inoculation

Reframing

Cognitive Restructuring

Relaxation Training

Progressive Relaxation

Deep breathing

Positive Imagery

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Pharmacotherapy

SSRI• Paroxetine (Paxil) only FDA for GAD• Fluoxetine (Prozac)• Sertraline (Zoloft)• Citalopram (Celexa)• Fluvoxamine (Luvox)

• See Table 11.4 in Kaplan & Saddock for dosing.

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Pharmacotherapy of Panic Disorder

SSRI

Paroxetine (Paxil)

Fluvoxamine (Luvox)

Sertraline (Zoloft)

DOSE

5-10 mg start

20-60 mg maintenance

12.5 mg start


12.5 – 25 mg start


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TCA

Clomipramine (Anafrinil)

Imipramine (Tofranil)

DOSE

5-12.5 mg start


10-12.5 mg start


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Benzodiazepines

Alprazolam (Xanax)

Clonazepine (Klonopin)

Lorazepam (Ativan)

DOSE

.25-.5 mg tid start

.5-2 mg tid maintenance

.25 -.5 mg bid start

.5-2 mg bid maintenance

25 -.5 mg bid start

.5-2 mg bid maintenance

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OBESSIVE-COMPULSIVE DISORDER

THEORY

DIAGNOSIS

TREATMENT

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OBSESSIONS

• INTRUSIVE THOUGHTS WISHES THAT CANNOT BE IGNORED, DISMISSED OR RESISTED.

• COMMON THEMES:

CONTAMINATION ORDERLINESS

VIOLENCE SEXUALITY

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COMPULSIONS COMMON FORMS

These behaviors or mental acts either are not connected in a realistic way with what they are designed to neutralize or prevent or are clearly excessive:

cleaning hand washing

ordering checking

touching counting

repeating words silently praying

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COMMOM OBSESSIONS & COMPULSIONS

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ASSESSMENT OF OCD

SCREENING TOOLS Yale-Brown Obsessive Compulsive Scale (YBOCS) Anxiety Screening Questionnaire (15 items) Primary Care Evaluation of Mental Disorders (PRIME-MD) Hamilton Anxiety & Depression Scale Beck Anxiety Scale Center for Epidemiological Studies Depression Scale (CESD) Hospital Anxiety & Depression Scale

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PSYCHOANALYTIC VIEW OF OBSESSIVE-COMPULSIVE DISORDER

OCD develops when child comes to fear his own ID impulses & uses EDMs as counter-thoughts or compulsive actions to lessen resulting anxiety.

Three ego-defenses are common in OCD:

isolation- isolates & disowns undesirable/unwanted thoughts & experiences them as intrusions

undoing - Individual engages in acts that implicitly cancel out their undesirable impulses.

reaction formation - Takes on lifestyle that directly opposes their unacceptable impulses.

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SEROTONIN & OBSESSIVE-CONPULSIVE DISORDER

• Serotonin plays role in operation of orbital region & caudate nuclei.

• Low levels of serotonin disrupts functioning. • Research has found:Reducing serotonin activity results in an

increase of OCD symptoms.Low levels of serotonin are related to high levels

of OCD symptoms.Increasing serotonin levels reduces symptoms.

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PHOBIC DISORDERS:SPECIFIC PHOBIASOCIAL PHOBIAAGORAPHOBIA

THEORY

DIAGNOSIS

TREATMENT

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SPECIFIC PHOBIASPECIFIC PHOBIA

A. Marked & persistent fear that is excessive or unreasonable, cued by presence or anticipation of a specific object or situation.

B. Exposure to phobic stimulus almost invariably provokes an immediate anxiety response

C. Person recognizes that the fear is excessive or unreasonable.

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SPECIFIC PHOBIASPECIFIC PHOBIA

.

Animal Type

Natural Environment Type (heights, storms, water)

Blood Injection Injury type

Situational Type (airplanes, elevators, enclosed places)

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AGE OF ONSET OF PHOBIA

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PSYCHOANALYTIC MODEL OF PHOBIC PSYCHOANALYTIC MODEL OF PHOBIC REACTIONSREACTIONS

• PHOBIAS ARE EXPRESSIONS WISHES/ FEARS WHICH ARE UNACCEPTABLE TO EGO

• UNCONSCIOUS CONFLICT IS DISPLACED TO EXTERNAL OBJECT OR SITUATION

• PHOBIA IS LESS THREATENING TO PERSON THAN THE RECOGNITION OF THE UNCONSCIOUS IMPULSE

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PSYCHOANALYTIC MODEL OF PHOBIC PSYCHOANALYTIC MODEL OF PHOBIC REACTIONSREACTIONS

PHOBIA IS ONLY A SYMPTOM OF UNDERLYING CONFLICT.

LEVEL OF PHOBIC FEAR INDICATES STRENGTH OF CONFLICT.

ONCE UNDERLYING CONFLICT IS DISPLACED ONTO EXTERNAL SITUATION, CONFLICT CAN BE CONTROLLED SIMPLY THROUGH AVOIDANCE.

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SOCIAL PHOBIASOCIAL PHOBIA

LIFE TIME PREVALENCE 11% MALES

15% FEMALESONSET IN ADOLESCENCE

COMMON IN FAMILIES WHO :

USE SHAME AS CONTROL TECHNIQUE

STRESS IMPORTANCE OF OPINIONS OF OTHERS

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CAN BE DIVIDED INTO 3 TYPES:

PERFORMANCE

LIMITED INTERACTIONAL

GENERALIZED

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PERFORMANCE

EXCESSIVE ANXIETY OVER ACTIVITIES

PLAYING INSTRUMENT

SPEAKING IN PUBLIC

EATING IN RESTAURANT

USING PUBLIC RESTROOM

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LIMITED INTERACTIONAL

EXCESSIVE FEAR ONLY IN SPECIFIC SOCIAL or VOCATIONAL SITUATIONS

ex. INTERACTING WITH AUTHORITY FIGURE

GOING OUT ON A DATE

SOCIAL PHOBIA

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SOCIAL PHOBIA

GENERALIZED

EXTREME ANXIETY DISPLAYED IN MOST SOCIAL SITUATIONS

MAY RESULT IN AVOIDANCE OF ALL SOCIAL INTERACTION

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AGORAPHOBIAAGORAPHOBIA

Anxiety about being in places or situations from which:

escape might be difficult (or embarrassing) OR help may not be available in the event of having an

unexpected or situationally predisposed Panic Attack or panic like symptoms.

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Agoraphobic fears typically involve characteristic clusters of situations that include:

being outside home alone

being in a crowd or standing in line

being on bridge

traveling in bus, train, or automobile.

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• LIFE TIME PREVALENCE 5% OF MALES & 12% OF FEMALES.

• DEVELOPS IN 50% OF PANIC DISORDERS

• FAMILY & TWIN STUDIES INDICATE 3-TO-5 TIMES GREATER RISK FOR PANIC DISORDER/ AGORAPHOBIA THAN IN GENERAL POPULATION

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• AFFECTS 1/2 OF VICTIMS BY AGE 8

• SOME MAY HAVE BEEN BORN WITH TENDENCY TOWARDS EXTREME SHYNESS

• 1-IN-5 DEMONSTRATED CONSISTENT FEAR & DISTRESS IN NOVEL SITUATIONS AS EARLY AS 8 WEEKS OF AGE.

• DISORDER THOUGHT TO OCCUR MORE OFTEN IN FEMALES BUT MALES

POST-TRAUMATIC STRESS DISORDER IN CHILDREN

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POST-TRAUMATIC STRESS DISORDERPOST-TRAUMATIC STRESS DISORDER

• MUST EXPERIENCE TRAUMATIC EVENT

• INTRUSIVE RE-EXPERIENCING OF EVENT

(DREAMS, FLASHBACKS, IMAGES, THOUHGTS, RECOLLECTIONS)

• AVOIDANCE OF STIMULI ASSOCIATED WITH EVENT

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PERCENTAGE OF INDIVIDUALS DX WITH PTSD

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• NUMBING OF RESPONSIVENESS TO THE WORLD & RESTRICTION OF AFFECT

• SYMPTOMS OF INCREASED AROUSAL

EXAGGERATED STARTLE REACTION

HYPERVIGILANCE

DIFFICULTY CONCENTRATING

INSOMINIA

NIGHTMARES

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• PTSD can occur at any age even childhood.

• In young people, the response may be expressed as agitated behavior.

• Most young people with PTSD avoid things that remind them of what happened.

• Many have physical symptoms as well, such as startling easily.

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PTSD IN CHILDRENPTSD IN CHILDRENETIOLOGICAL FACTORSETIOLOGICAL FACTORS

• Certain PREMORBID personality profiles & attitudes are more likely to develop PTSD.

• Pre-morbid personality or psychological difficulties are associated with increase risk & more severe ASD & PTSD symptoms:

poor interpersonal relationships external locus of control pessimism

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ETIOLOGICAL FACTORS

• NATURE & QUALITY OF SOCIAL SUPPORT SYSTEM

• Person with a strong social support system after a traumatic event less likely to develop an extended disorder.

• If feels loved/accepted/valued, will be more likely to recover.

• Societal support for appears to be important in lessening severity & duration of symptoms.

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ETIOLOGICAL FACTORS ETIOLOGICAL FACTORS

• DEGREE OF EXPOSURE & SUBJECTIVE EXPERIENCE OF THREAT PLAYS CRITICAL ROLE IN DEVELOPMENT OF PTSD & ASD.

• DURATION OF THE EXPOSURE

• LEVEL OF INVOLVEMENT

• SALIENCE

• DEGREE OF HARM EXPERIENCED

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MIXED ANXIETY & DEPRESSIONMIXED ANXIETY & DEPRESSION

• SHARED SYMPTOMS

• EXCESSIVE WORRY

• MOTOR TENSION

• EASY FATIGABILITY

• DIFFICULTY CONCENTRATING

• SOMATIC COMPLAINTS

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MIXED ANXIETY & DEPRESSION

• ANXIETY

• SHORTNESS OF BREATH

• CHEST PAIN• NERVOUSNESS• IRRITABILITY• BURNING STOMACH• DIFFICULTY FALLING

ASLEEP

• DEPRESSION

• DEPRESSED MOOD• ANHEDONIA• WEIGHT LOSS OR

GAIN• SUICIDAL

THOUGHTS• EARLY MORNING

AWAKENING

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MEDICATIONS THAT REDUCE ANXIETYMEDICATIONS THAT REDUCE ANXIETY

• AZASPIRONES

BUSPRIONE BUSPAR

• BETA BLOCKERS

PROPANOLOL INDERAL

ATENOLOL TENORMIN

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ANXIETY DISORDERS IN PRIMARY CARE: ANXIETY DISORDERS IN PRIMARY CARE: GUIDELINESGUIDELINES

• RECOGNIZE ANXIETY AS CAUSE OF PT’s PRESENTING SYMPTOMS:

LOOK FOR MULTIPLE SYMPTOMS

GREATER # OF PHYSICAL SYMPTOMS, MORE LIKELY ANXIETY D/O PRESENT

GREATER # OF SOMATOFORM SYMPTOMS, MORE LIKELY ANXIETY D/O PRESENT

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ANXIETY DISORDERS IN PRIMARY CARE: GUIDELINESANXIETY DISORDERS IN PRIMARY CARE: GUIDELINES

RECOGNIZE ONLY A SMALL NUMBER OF PT’S WITH ANXIETY SYMPTOMS ARE A RESULT OF GENERAL MEDICAL CONDITION.

LOOK FOR ANXIETY IN OTHER LIFE AREAS

LOOK FOR TRIGGERS OR AVOIDANCE (TIME/PLACE/SETTING/CONTEXT)

LOOK FOR MULTIPLE SYMPTOMS

LOOK FOR SOMATOFORM SYMPTOMS

EPIDEMIOLOGY = APPEARS IN YOUNGER PT--> LESS RISK FOR ILLNESS

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ANXIETY DISORDERS IN PRIMARY CARE: ANXIETY DISORDERS IN PRIMARY CARE: GUIDELINESGUIDELINES

• A SIGNIFICANT # OF PT’S WITH ANXIETY SYMPTOMS HAVE CO-MORBID PSYCHIATRIC DISORDERS.

• 26% SUFFER FROM 2 OR MORE INDEPENDENT ANXIETY DISORDERS. 55% SUFFERED FROM MULTIPLE DISORDERS, ONE OF WHICH HELPED CAUSE THE OTHERS.

• MAJOR DEPRESSION

• SUBSTANCE DEPENDENCE/ ABUSE

Documents

Anxiety disorders in adults 2005