anxiety.ppt

Anxiety Disorders

Anxiety• Fear is an emotional and physiological response to a

recognized external threat (e.g. A speeding car or the steep descent in an airplane).

• Anxiety is a state of apprehension, uncertainty, and fear resulting from the anticipation of a realistic or fantasized threatening event or situation, often impairing physical and psychological functioning.

• Anxiety is the subjective experience of fear and its physical manifestations.

• Because fear of recognized threats causes similar unpleasant mental and physical changes, the two terms are usually used interchangeably.

Anxiety is a common and normal response to a perceived threat.

Need to distinguish normal from pathological. Pathological Anxiety Inappropriate Either no real source of fear or the source is

not sufficient to account for the severity of symptoms.

Symptoms interfere with daily functioning and interpersonal relationships/work.

Anxiety

• Intensity varies from minor qualms to noticeable trembling to its most extreme form panic.

• Course also varies with a peak severity being reached within a few seconds or more gradually over minutes, hours or days.

• Duration also varies from a few seconds to hours or even days or months, although episodes of panic usually abate within ten minutes and seldom last more than thirty minutes.

Anxiety

Anxiety may arise:• Unexpectedly ( out of the blue) – called

spontaneous anxiety or spontaneous panic if intense.• Predictably in specific situations – called phobic or

situational panic.• Anticipatory anxiety or panic – anxiety triggered by

the mere thought of particular situations.

Anxiety and Depression• At least three-fourths of patients with primary

depression complain of feeling anxious, worried, or fearful. Extreme anxiety may occur in agitated depression in the form of anguished facial expression, lip biting, picking at fingers, nails or clothing, hand wringing, constant pacing and inability to sit quietly.

• Primary anxiety can be depressing. If it persists, and particularly if it interferes with functioning secondary depression is the rule rather the exception.

Pathophysiology of anxiety• The neurocircuitry of anxiety has been postulated to arise

from the amygdala, the brain area that registers the emotional significance of environmental stimuli and stores emotional memories.

• The efferent pathways from the central nucleus of the amygdala travel to a multiplicity of critical brain structures, including the parabrachial nucleus (resulting in dyspnea and hyperventilation), the dorsomedial nucleus of the vagus nerve and nucleus ambiguous (activating the parasympathetic nervous system), and the lateral hypothalamus (resulting in SNS activation).

Through reciprocal neuronal pathways connecting the amygdala to the medial prefrontal cortex, cognitive experience of the specific anxiety disorder differs, although fear symptoms may overlap.

• Panic attacks the fear is of imminent death; • Social phobia, the fear is of embarassment;• Postraumatic stress disorder, the traumatic memory

is remembered or reexperienced; • Obsessive-compulsive disorder, obsessional ideas

recur and intrude; • Generalized anxiety disorder, anxiety is “free-

floating” (i.e., not conditioned to specific situations or triggers).

• Anxiety disorders appear to be caused by an interaction of biopsychosocial factors, including genetic vulnerability, which interact with situations, stress, or trauma to produce clinically significant syndromes.

• Hyperresponsiveness of the amygdala may relate to reduced activation thresholds when responding to perceived social threat.

• Prefrontal-limbic activation abnormalities have been shown to reverse with clinical response to psychologic or pharmacologic interventions.

• In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA).

• Positron emission tomography (PET) scanning has demonstrated increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients with panic disorder.

• Research and treatment trials suggest that abnormalities in serotonin neurotransmission in the brain are meaningfully involved in obsessive-compulsive disorder (OCD). This is strongly supported by the efficacy of serotonin reuptake inhibitors in the treatment of OCD.

• Evidence also suggests abnormalities in dopaminergic transmission in at least some cases of OCD.

Anxiety Disorders

• Panic Disorder• Agoraphobia• Specific Phobia• Social Phobia• Obsessive Compulsive Disorder• Generalized Anxiety Disorder• Post-Traumatic Stress Disorder• Acute Stress Disorder

• Anxiety disorder due to general medical condition

• Substance Induced anxiety disorder• Anxiety Disorder not otherwise specified

Anxiety Disorder due to general medical condition

Causes:• Hyperthyroidism• Vitamin B12 deficiency• Hypoxia• Neurological disorders (epilepsy, brain tumors, multiple

sclerosis)• Cardiovascular disease• Anemia • Pheochromocytoma• Hypoglycemia

DSM 1V Criteria

• Prominent anxiety, panic attacks, or obsessions or compulsions predominate the clinical picture.

• There is evidence from the history, PE or lab findings that the disturbance is the direct physiological consequence of a general medical condition.

• The disturbance is not better accounted for by another mental disorder.

• The disturbance does not occur exclusively during the course of a delirium.

• The disturbance causes clinically significant distress or impairment in social, occupational or other areas of functioning.

Substance-induced Anxiety Disorder

• Caffeine intake and withdrawal• Amphetamines• Alcohol and sedative withdrawal• Other illicit drug withdrawal• Mercury and arsenic toxicity• Organophosphate or benzene toxicity• Penicillin• Sulphonamides • Sympathomimetics • Antidepressants

Panic Disorder

• Panic attacks are discrete periods of heightened anxiety that classically occur in people with panic disorder but can also occur in other conditions, especially, phobic disorder and posttraumatic stress disorder.

• Panic attacks peak and abate within ten minutes. Rarely they last more than one hour.

Panic attack, DSM 1V criteriaA discrete period of intense fear and discomfort that is accompanied by at least four of the following: • Palpitations• Sweating• Shaking• Shortness of breath • Choking sensation • Chest pain• Nausea • Light headedness

• Depersonalization • Fear of losing control or

“going crazy”• Fear of dying• Numbness or tingling• Chills or hot flashes

Panic Disorder

Characterized by experience of panic attacks accompanied by persistent fear of having additional attacks.

DSM IV Criteria for Panic Disorder A) Both (1) and (2) (1) recurrent unexpected Panic Attacks (2) at least one of the attacks has been followed by 1 month (or more) of one (or

more) of the following:(a) persistent concern about having additional attacks(b) worry about the implications of the attack or its consequences (e.g., losing

control, having a heart attack, "going crazy")(c) a significant change in behavior related to the attacks B) The Panic Attacks are not due to the direct physiological effects of a substance

(e.g., a drug of abuse, a medication) or a general medical condition (e.g., hyperthyroidism).

C) The Panic Attacks are not better accounted for by another mental disorder, such as Social Phobia (e.g., occurring on exposure to feared social situations), Specific Phobia (e.g., on exposure to a specific phobic situation), Obsessive-Compulsive Disorder (e.g., on exposure to dirt in someone with an obsession about contamination), Posttraumatic Stress Disorder (e.g., in response to stimuli associated with a severe stressor), or Separation Anxiety Disorder (e.g., in response to being away from home or close relatives).

Presentation• First attack- usually unexpected, but may

follow a period of stress.• Subsequent attacks occur spontaneously but

may be associated with specific situations.• On average they occur 2x per week but may

range from several times per day to a few times per year.

• Anticipatory anxiety between periods is common.

Panic inducing Substances

• Induce panic in patients with panic disorder and in some people without panic disorder.

Includes: • Intravenous sodium lactate• Hyperventilation – decreases blood CO2,

ionized calcium and phosphorus produces paresthesias, lightheadedness, visual changes, and feelings of unreality that contribute to the fear of fainting.

Epidemiology

• Lifetime prevalence : 2 – 5%• 2 to 3 times more common in females than

males• Strong genetic component: four to eight times

greater risk of panic disorder if first degree relative is affected.

• Onset usually from late teens to early thirties (average 25)

Associated conditions

• Following conditions are both associated with panic disorder and agoraphobia:

1.Major depression (40-80%)2.Substance dependence (20-40%)3.Social and specific phobias4.Obsessive compulsive disorder

Course and Prognosis

• Variable course, often chronic.• Relapses common with discontinuation of

medical therapy:10-20% continue to have significant symptoms

that interfere with daily life.50% continue to have mild symptoms30-40% remain symptom free after treatment.

Treatment

• Psychological• Behavior therapy• Drug therapy

Drug therapy

• Acute initial treatment of anxiety Benzodiazepines (only short course,

dependence). Dose may be tapered as SSRI are added (anxiolytic).

SSRI- are drugs of choice Take 2-4 weeks to become effective. Other antidepressants may be used. treatment should continue for 8-12 months.

Agoraphobia• Always specify panic disorder with agoraphobia or

without agoraphobia.• Agoraphobia is the fear of being alone in public

places. It often develops secondary to panic attacks due to apprehension about having subsequent attacks in public places where escape or needed help may be difficult.

• Can be diagnosed alone or with panic disorder.• 50-75% of patients have coexisting panic disorder.

DSM-IV Diagnostic Criteria for AgoraphobiaA) anxiety about being in places or situations from which escape might be

difficult (or embarrassing) or in which help may not be available in the event of having an unexpected or situationally predisposed Panic Attack or panic-like symptoms. Agoraphobic fears typically involve characteristic clusters of situations that include being outside the home alone; being in a crowd, or standing in a line; being on a bridge; and traveling in a bus, train, or automobile.

B) The situations are avoided (e.g., travel is restricted) or else are endured with marked distress or with anxiety about having a Panic Attack or panic-like symptoms, or require the presence of a companion.

C) The anxiety or phobic avoidance is not better accounted for by another mental disorder, such as Social Phobia (e.g., avoidance limited to social situations because of fear of embarrassment), Specific Phobia (e.g., avoidance limited to a single situation like elevators), Obsessive-Compulsive Disorder (e.g., avoidance of dirt in someone with an obsession about contamination), Posttraumatic Stress Disorder (e.g., avoidance of stimuli associated with a severe stressor), or Separation Anxiety Disorder (e.g., avoidance of leaving home or relatives).

Relationship bet. Panic attacks and agoraphobia

• Clinical scenario: a person who has a panic attack while shopping in a large supermarket subsequently develops a fear of entering that supermarket. As the person experiences more panic attacks in different settings, they develops a progressive and more general fear of public spaces (agoraphobia).

Treatment

• Psychological • Behavioral • Drug treatment

Drug treatment

• When panic is present : as you treat panic agoraphobia goes away

• When agoraphobia alone : behavioral therapy. Behavioral therapy and anxiolytics. When agoraphobia occurs alone it is usually

chronic and debilitating.

Specific and Social Phobia• A phobia is defined as a persistent irrational fear

that leads to avoidance of the feared object or situation.

• A specific phobia is a strong, exaggerated, persistent, irrational fear of a specific object or situation.

• A social phobia is a fear of social situations in which embarrassment can occur.

DSM Specific Phobia

DSM Social Phobia

Common Specific Phobia

Fear of :• Animals• Heights• Blood or needles• Illness or injury• Death

Common Social Phobia

Fear of :• Speaking in public• Eating in public• Using public restrooms

Epidemiology • Most common mental disorders in the US• Affects approximately 5-10% of the

population• Specific phobia more common than social

phobia• For specific phobias onset may be as young as

five years old for phobias such as seeing blood and as old as 35 for situational fears (heights).

• Average age of onset for social phobias is mid teens.

Course and prognosis

• Not clearly defined

Treatment • Specific phobias Pharmacological treatment has not been found

effective. Systemic desensitization, with or without hypnosis, and supportive psychotherapy are often useful. If necessary a short course of benzodiazepines or beta blockers may be used during desensitization to help control autonomic symptoms.

Systemic desensitization: gradually expose patient to a feared object or situation while teaching relaxation and breathing techniques.

Social phobia

• Paroxetine, an SSRI, has been approved by the FDA for treatment of.

• Beta blockers are frequently used to control symptoms of performance anxiety.

• Cognitive and behavioral therapy are useful adjuncts.

OBSESSIVE COMPULSIVE DISORDERMovies: The Aviator, As Good As It Gets

OCD• Diverse group of symptoms that include recurring,

intrusive thoughts, rituals, preoccupations and repetitive behaviours that are time consuming and interfere significantly with function

• Either or both– Obsessions = mental event

• Recurrent and intrusive thoughts, feelings, ideas or sensations– Compulsions = behaviour

• Conscious, standardized, recurrent behaviours (e.g. counting, checking, avoiding)

• Sequence of events (generally)– Obsessions Anxious dread Compulsions to decrease

anxiety

DSM-IV: OCDA. Either obsessions or compulsions:

– Obsessions defined by 1, 2, 3 and 41) Recurrent and persistent thoughts/impulses/images experienced at times

as intrusive and inappropriate anxiety/distress2) Not just excessive worries about real life problems3) Attempts to ignore/suppress thoughts, impulse, or images, or to neutralize

with other thought/action4) Recognized as product of own mind (not imposed from without as in

thought insertion)– Compulsions defined by 1 and 2

1) Repetitive behaviours (e.g. hand washing, ordering, checking) or mental acts (e.g. praying, counting, repeating words silently) that person feels driven to perform in response to obsession, or according to rigidly applied rules

2) Aims to prevent/reduce distress, or dreaded situation/event. Behaviours/mental acts not connected in realistic way or are excessive to what they are designed to prevent/neutralize

B. Recognition that obsessions/compulsions are unreasonableC. Marked distress, time consuming (>1 hour/day), or significant interferenceD. Obsession or compulsion not restricted to another Axis I d/o

– E.g. preoccupation with food in presence of eating d/o, hair pulling in trichotillomania, appearance concern in body dysmorphic d/o

E. R/o substances or general medical condition

Epidemiology

• Lifetime prevalence– 2 – 3 %– Male = female (adults), male > female

(adolescents)

• Mean age of onset 20 yo– younger onset in men– 2/3 patients have onset by 25 yo– <15% onset after 35 yo

Comorbidity• Major depressive d/o

– Lifetime prevalence 67%• Social phobia

– Lifetime prevalence 25%• ADHD• Alcohol and other substance d/o• Generalized anxiety d/o• Specific phobias• Panic d/o• Eating d/o• Personality d/o• Tourette’s

– Incidence 6 – 7%• Tics

– 20 – 30% patients with OCD have history of this

Etiology

• Biological– Neurotransmitters: 5-HT dysfunction– Imaging:

• Increased activity of corticostriatal pathways– PET: orbitofrontal, basal ganglia (especially caudate), cingulum

• Decreased size of caudate bilaterally (MRI)» Reverses with treatment

• Genetics– 3-5x increased risk OCD if 1st degree relative with OCD– Increased risk OCD if 1st degree relative with Tourettes

• Linkage b/w Tourette’s, chronic motor tics and OCD

Etiology: Psychological• Learning theory:

– Obsessions: conditioned response• Neutral stimuli (thoughts) + anxiety/noxious response noxious

interpretation of neutral stimuli– Compulsions: reinforced, learned pattern of avoidance

• Interruption of this anxiety• Psychodynamic:

– Magical thinking: omnipotence of thought• Thinking about event event occurring

– E.g. thinking about parent dying parent dying– Skips over action needed for event to occur

– Overvaluation of thought• Perceive thoughts as powerful wishes = deeds

– E.g. violent thoughts = violent acts “I’m a violent person”– Dynamics supporting OCD

• Stressful life events can trigger symptoms• Interpersonal conflict• Maintaining symptoms for 2o gain

Etiology: Psychological• Cognitive theories:

– Excessive sense of responsibility• Non-OCD: intrusive thoughts/impulses = trash• OCD: intrusive thoughts/impulses = something dangerous

– increased anxiety/depression– Increased focus on intrusive thoughts– attempts to counteract/neutralize thoughts

» E.g. compulsions, avoidance, reassurance-seeking– “Fusion”

• Obsessional thought morally equivalent to activity in thought guilt and anxiety– E.g. thinking of hurting small child as immoral as actually hurting

child– Other assumptions in OCD

• Having thought = performing action• Failing to prevent harm to self/others = causing harm in 1st place• Not neutralizing thoughts = seeking/wanting harm to happen• One can exercise control over own thoughts Belief that thoughts

can be completely controlled

Clinical features

• Concealment of symptoms– 5-10 years untreated illness before presenting to Ψ– Often present to other specialists first

• Reassurance seeking about basic fears– E.g. “Did I wash properly?” “Did I put glass in the food?”

reassurance transient comfort cycle starts over• Obsessions, compulsions together/alone

– 75% have both obsessions and compulsions– 5 - 25% “pure obsessions” without compulsions– In chronic OCD – may have compulsions in absence of provoking

thought• Behaviour performed “out of habit”

• Obsessions/compulsions can change over time

Screening Questions• Compulsions: – Do you ever have to perform a behaviour or repeat some

action that doesn’t make sense to you or that you don’t want to do?

– For example, washing or cleaning excessively, checking things over and over, counting things repeatedly?

• Obsessions:– Do you experience disturbing thoughts, images, or urges

that keep coming back to you and that you have trouble putting out of your head?

– For example, being contaminated by something, something terrible happening to you or someone you care about, or of doing something terrible?

Symptom Patterns1. Contamination (“cleaners”)– Obsession: contamination Compulsion: hand washing, avoidance– Usually of hard to avoid material (bodily secretions, dust, germs)

2. Pathological doubt (“checkers”)– Obsession: danger Compulsion: checking– Usually some perception of violence/danger• E.g. stove, door

3. Repetition obsessions/compulsions (“counters”/”repeaters”)– Compulsion: continue repeating an action until done “correctly”

4. Intrusive thoughts (“pure obsessions”)– Obsessions: sexual, religious or aggressive acts repulsive to pt– Usually without compulsions

5. Orderliness– Compulsion: symmetry, precision

6. Hoarding– Obsession: throwing away something valuable Compulsion: holding on to

clutter/garbage7. Other– Compulsions: trichotillomania (hair pulling), nail biting, masturbating,

compulsive slowness

“Sounds like an obsessive-compulsive disorder. Normal people don’t spend that much time washing their hands.

Differential Diagnosis

Course and Prognosis• Variable course:– Episodic vs. constant symptoms

• Prognosis– 2/3 improve, 1/3 same or worsen– Negative factors

• Poor insight, poor resistance of compulsions, bizarre compulsions

• Childhood onset, hospitalization• Comorbid MDD, personality d/o, delusions, overvalued ideas

– Positive factors• Good social/occupational adjustment• Onset associated with precipitating event• Episodic course

– Not influenced by obsessional content

Treatment: Pharmacotherapy

• Start with low doses and increase gradually

• 1st line:– SSRI: fluvoxamine, fluoxetine, paroxetine,

sertraline• 2nd line:– TCA: Clomipramine (gold standard)– Other antidepressants: venlefaxine XR,

citalopram, mirtazepine– Adjunct: Risperidone

Treatment: Pharmacotherapy• If poor response:

– Optimize dose first for at least 10 - 12 week trial• Generally higher response rates at upper end of therapeutic range

– If no improvement, switch to another 1st line agent before moving to 2nd line

– Consider adjunctive therapy with 2nd or 3rd line agent early

• For treatment-refractory OCD: – Review for comorbid psychiatric/medical conditions– Consider 3rd Line:

• Antidepressants: IV clomipramine, escitalopram, phenelzine, tranylcypromine

• Adjunct: mirtazepine, olanzepine, quetiapine, haloperidal, gabapentin, topiramate, tramadol, riluzol, St. John’s Wart, pindolol

• Medications not recommended:– Clonazepam, dispramine, bupropion, lithium, naltrexone, adjunctive

morphine

Treatment: Pharmacology• Duration:

– Initial response at 6 weeks– Should continue for 12 – 24 months, however most require

lifelong treatment• But continue for at least 6 months

• Discontinuation:– High risk of relapse on d/c of medications

• 35-40% relapse within 6 months• 88% relapse even after 2 years stable on medications

– Not generally advised– Studies comparing CBT to medications showed decreased risk of

relapse in CBT group following d/c

Treatment: Psychotherapy• As effective as pharmacotherapy• Longer lasting than pharmacotherapy on discontinuation

• CBT– Education– Exposure

• In vivo and imaginary to anxiety provoking situations, compulsions and obsessions

• Develop tolerance vs.. avoidance to anxious stimuli– Response prevention

• Compulsive behaviours, reassurance seeking and excessive safety behaviours– Cognitive interventions

• Correct misperceptions around danger, omnipotence of thought, excessive responsibility

• Learn to tolerate uncertainty and decrease perfectionism– Family involvement– Problem solving– Relapse prevention

Treatment:• Reserved for severe treatment refractory OCD

• ECT– Not as effective as neurosurgery

• Deep Brain Stimulation– “Brain pacemaker” used in epilepsy, Parkinson’s, essential tremor– Bilateral indwelling electrodes in anterior limb of internal capsule

• Improvement in O-C symptoms, mood, anxiety

• Psychosurgery– Procedures: anterior cingulotomy, anterior capsulotomy, tractomy,

limbic leucotomy– 25-30% efficacy of treatment refractory OCD– Seizures are most common complication

GENERALIZED ANXIETY DISORDER

GAD• Indiscriminate, uncontrollable, excessive worry

about “everything” accompanied by somatic distress that is disabling and causes significant dysfunction

• 2 components:1. Worry about several life circumstances2. Somatic distress (tension, nervousness,

hyperarousal)

• Vs. situation crisis– Worry is restricted to one situational problem

DSM-IV: GAD

A. 6 months of excessive worry and anxiety about a number of events/activities

B. Difficult to control worryC. 3/6 symptoms:

1) Tension in muscles2) Concentrating difficulties or mind going blank3) Irritability (Hyperarousal)4) Energy loss5) Restlessness, feeling keyed up, or on edge6) Sleep disturbance

D. Focus of worry not confined to other Axis I d/oE. Significant distress or impairmentF. R/o substances, GMC, mood d/o, psychotic d/o or pervasive

development d/o

Epidemiology

• Lifetime prevalence– US comorbidity study: 5 %• Female (6.6%) : Males (3.6%) 2:1

– WHO: 8%

• Typical age of onset: late teens, early adulthood

Comorbidity

50 – 90% GAD sufferers have comorbidities

• Major depression/dysthymia (50 – 75%)• Panic d/o (25%)• Social phobia (23 – 30%)• OCD• Substance use d/o• Personality d/o (30 – 60%)– Especially cluster C

Differential dx 1 (= Panic)

Differential dx 2

Etiology: Biological

• Findings somewhat contradictory, however• Neurotransmitters

• 5-HT dysfunction• GABA dysfunction

– ? occipital lobe b/c of high density of BZD receptors• Imaging

• ? Inverse relationship b/w anxiety and metabolic activity– PET: decreased metabolic rate of basal ganglia/white matter– Decreased activity in occipital areas, R prefrontal cortex, R post temporal

lobe, cerebellum– Inc/Dec activity in cortical/limbic and basal ganglia areas

• Genetics– Concordance 50% MZ vs. 15% DZ twins– 25% risk if 1st degree relative has GAD

Etiology: Psychosocial

• Cognitive models– Negatively biased view of world

• Selective attention to negative/threat cues in environment– Overestimate probability of negative event occurring– Catastrophic thinking

• Extreme conclusions for relatively minor events– Sense of inadequacy to cope/control outcome

• Psychodynamic– Anxiety is symptom of unconscious, unresolved conflict

Course and Prognosis

• Fluctuating– Different symptoms and severity over time

• Impairment– Epidemiological catchment area survey• 30% on disability• 50% working• 3x more likely to be working at lower occupational

level

Screening Questions

• What kinds of things do you worry about?• Do you worry excessively about everyday things

such as your family, health, work, or finances? • Do friends or loved ones tell you that you worry

too much? • Do you have difficulty controlling your worry,

such that the worry keeps you from sleeping or makes you feel physically ill with headaches, stomach troubles or fatigue?

Treatment: Targets

1. Co-Morbid conditions– Antidepressant, cognitive therapy

2. Worry (negative expectations)– Cognitive therapy, antidepressants, distraction

3. Somatic distress from hyper-arousal– Relaxation training, aerobic exercise, Rx

Treatment: Pharmacotherapy

• Start with low doses and increase gradually

• 1st line:– SSRI: paroxetine, escitalopram, sertraline– SNRI: venlefaxine XR

• 2nd line:– BZD: alprazolam, bromazepam, lorazepam,

diazepam• For acute GAD on time-limited basis, not indefinitely

– Buspirone, imipramine, bupropion XL, pregabalin

Treatment: Pharmacotherapy• If poor response:– Optimize dose first – If no improvement, switch to another 1st line agent before

moving to 2nd line

• For treatment-refractory GAD: – Review for comorbid psychiatric/medical conditions– Consider 3rd Line:

• Mirtazapine, citalopram, trazodone, hydroxyzine • Adjunctive: olanzapine, risperidone

• Medications not recommended:– Propranolol

Treatment: Pharmacology• Duration:

– Significant response by 6 – 12 weeks• Some patients report some improvement at 1 week

– Should continue for at least 1 year, however most require lifelong treatment

• Discontinuation:– High risk of relapse on d/c of medications

• 25% relapse within 1 month• 60 - 80% relapse within 1 year

– Not generally advised– Studies comparing CBT to medications showed decreased risk of

relapse in CBT group following d/c

Treatment: Psychotherapy• As effective as pharmacotherapy• Longer lasting than pharmacotherapy on discontinuation• CBT

– Education– Cognitive interventions

• Correct unrealistic beliefs about worry (e.g. that it helps problem solving, shows caring, prepares for misfortune)

• Develop more realistic thoughts around catastrophic thinking, etc.– Exposure

• Imaginary exposure to worry-related imagery and catastrophic situations• Practice eliminating unrealistic safety behaviour (e.g. excessive reassurance seeking,

having family members call all the time)– Emotional regulation

• Relaxation techniques, mindfulness-based meditation• Learn to tolerate anxiety

– Problem solving• Sleep hygiene, time management , procrastination, avoidance• Deal with interpersonal conflicts• Increase pleasurable activities and focus on life goals

– Relapse prevention

POSTTRAUMATIC STRESS DISORDER

History (1)• “Irritable heart syndrome”– US Civil War – Soldiers generalized weakness, palpitation, CP

and heaviness, SOB, sweating, GI changes– Thought to be cardiac origin

• “Shell Shock”– WWI– Brain damage from exploding shells

History (2)• “Combat Neurosis”, “Operational fatigue”– Emphasized pre-trauma characteristics

• Re-activation of early developmental conflicts

– 15 – 20 yr follow up study (Archibald, 1962)• Disabling condition involving startle response, sleep

changes, dizziness, blackouts, avoidance or activities like combat and internalization of feelings

• “Post-Traumatic Stress disorder”– Vietnam War– Renewed interest in war-related psychiatric d/o– Political/economic pressure inclusion on DSM-III

PTSD

• Development of symptom cluster after exposure to traumatic life event of painful re-experiencing, avoidance and emotional numbing and constant hyperarousal.

• Basic elements:A. Traumatic stressB. Intrusive recollectionsC. Avoidance and numbingD. Increase arousal

DSM-IV (1)A. Exposure to traumatic event with both of

1) Experience, witness or confronted with event that involved actual or threatened death/serious injury, or physical threat to self/others

2) Intense fear, helplessness or horrorB. Persistent reexperience in 1/5 ways

1) Intrusive recollections (images, thoughts, perceptions)2) Recurrent distressing dreams3) Acting/feeling as if event recurring (sense of reliving, illusions, hallucinations,

dissociative flashbacks)4) Intense psychological distress to internal/external cues5) Physiological reactivity to internal/external cues

C. Avoidance of stimuli and numbing of responsiveness with 3/71) Avoid thoughts, feelings, or conversations2) Avoid activities, places, or people3) Inability to recall important aspect of trauma4) Markedly diminished interest in activities5) Feeling of detachment or estrangement from others6) Restricted range of affect (e.g. unable to have loving feelings)7) sense of foreshortened future (e.g. does not expect to have a career,

marriage, children, or normal life span)

DSM-IV (2)D. Persistent increased arousal with 2/5

1) Sleeplessness (falling or staying asleep)2) Irritability3) Concentration difficulties4) Hypervigilance5) Exaggerated startle response

E. >1 month of B, C, and DF. Significant distress or functional impairment

Specify ifAcute: < 3 months durationChronic: >3 months duration

Specify ifDelayed onset: symptom onset >6 months after stressor

Screening Questions

• Are you bothered by memories, thoughts, or images of a very upsetting event that happened to you or someone close to you in the past?

• For example: – Being in a fire or serious accident? – Being raped, assaulted, or abused? – Seeing someone else badly hurt or killed?

Epidemiology

• Lifetime prevalence in general population 8%– Females (10%) : Males (5%)

• Females: assault/rape, Males: combat

– Subclinical PTSD 5 – 15%

• Greater prevalence in high-risk groups– Vietnam veterans: 30 % PTSD, 25% subclinical– Rape victims: 1 month after >50%, 1 year 25%, several

years 5 – 10%

• Generally 25% of those exposed to DSM-IV criterion type events develop PTSD

Etiology: Biological

• Neurotransmitters– Hyperactivity of NA, endogenous opiate systems– Hypersensitivity of HPA Axis/Decreased cortisol

• Structures involved– Amygdala

• Integrates sensory information + emotional tone + neuromodulation for memory consolidation

– Hippocampus• Organize memory• Extreme stress disrupts hippocampal function so that

memory is stored as an affective state or as sensory fragments

Etiology: Psychosocial• Psychodynamic– Trauma reactivates prior quiescent, unresolved

psychological conflict• Cognitive model– Difficulty processing/rationalizing trauma or coping with

effects – Experience kept alive as a memory pain reexperienced – Attempts to avoid/deny to decrease anxiety

• Behavioural model– Trauma + intense fear paired with conditioned stimulus

(internal or external - smells, sights, sounds)– Conditioned stimulus elicits fear alone– Avoidance of both unconditioned and conditioned stimuli

Comorbidity

• 2/3 develop at least 2 other disorders– Depressive d/o– Substance-related d/o– Anxiety d/o– Bipolar d/o

• Comorbid d/o increase risk of PTSD

Differential Diagnosis• Psychiatric– Other anxiety d/o (panic, GAD)– Major Depressive d/o– Alcohol or substance-use d/o– Acute intoxication or withdrawal– Phobias– Personality d/o (especially borderline PD)– Factitious d/o– Dissociative d/o– Schizophrenia– Adjustment disorder

• If stress has not been meaningfully/significantly traumatic

Course and Prognosis

• Typically delay in symptom onset– Short as 1 week

• Symptoms fluctuate over time– May intensify with acute stress

• If untreated:– Full recovery 30%, at 1 year 50%– Mild symptoms 40%– Moderate symptoms 20%– Unchanged or worse symptoms 10%

Good Prognostic Factors

• Rapid onset of symptoms• Short duration of symptoms• Good premorbid functioning• Strong social supports• Absence of other psychiatric/substance/medical

d/o• No other risk factors

Treatment: Pharmacotherapy

• Start with low doses and increase gradually

• 1st line:– SSRI: fluoxetine, paroxetine, sertraline– SNRI: venlefaxine XR

• 2nd line:– Antidepressant: fluvoxamine, mirtazapine,

moclobemide, phenelzine– Adjunctive: risperidone, olanzapine

Treatment: Pharmacotherapy• If poor response:– Check compliance– Optimize dose first – If no improvement, switch to another 1st line agent before

moving to 2nd line

• For treatment-refractory PTSD: – Review for comorbid psychiatric/medical conditions– Consider 3rd Line:

Amitriptyline, imipramine, escitalopram Adjunctive: carbamazepine, gabapentin, lamotrigine,

valproate, tiagabine, topiramate, quetiapine, clonidine, trazodone, buspirone, bupropion, prazosin, citalopram, fluphenazine, naltrexone

Treatment: Pharmacology• Duration:

– Some response with SSRIs by 2 – 4 weeks; trial is 8 weeks– Some studies show improvement up to 36/52

Sertraline: ½ non-responders as 12/52, responded by 36/52– Chronic PTSD: continue for at least 1 year

• Discontinuation:– High risk of relapse on d/c of medications

• 25% relapse within 6 months• But relapse rate is generally lower than untreated patients

– Studies of CBT showed more sustained benefit in CBT group following d/c at 6 – 18/12

Treatment: Psychotherapy• CBT

– Education– Emotional regulation

Management skills to help cope and reduce distress• Relaxation techniques such as muscle, breathing and imagery • Practice acceptance based approaches to reduce avoidance of difficult emotions

– Exposure• Confront feared situations, memories, emotions until distress is significantly

diminished• Imaginal exposure to repeatedly review trauma based on memories of event

including emotions• In vivo exposure by confronting avoided situations

Cognitive interventions• Identify dysfunctional thinking patterns associated with anxiety, depression, anger,

shame• Challenge irrational cognitions and replace them with functional, realistic beliefs

– Problem solving• Overcome social withdrawal and negative impacts on relationships• Address excessive substance use or unhealthy coping methods• Encourage positive activities and goals

– Relapse prevention