April 9, 2014 Elliott K. Lee MD, FRCP(C) Staff Psychiatrist Anxiety Disorders Clinic Royal Ottawa...
-
Upload
evelyn-palk -
Category
Documents
-
view
221 -
download
3
Transcript of April 9, 2014 Elliott K. Lee MD, FRCP(C) Staff Psychiatrist Anxiety Disorders Clinic Royal Ottawa...
April 9, 2014
Elliott K. Lee MD, FRCP(C)
Staff Psychiatrist
Anxiety Disorders Clinic
Royal Ottawa Mental Health Centre
Anxiety DisordersBack to Basics
Anxiety results from an unknown internal stimulus, or is inappropriate or excessive when compared to the existing external stimulus.
It is an expected, normal and transient response to stress; may be a necessary cue for adaptation and coping (future event)
Different from Fear:sense of dread/foreboding that occurs in response to external threatening event.
Anxiety
Pathologic anxiety1. Autonomy: i.e. Minimal/no recognizable
environmental trigger2. Intensity – exceeds tolerance capacity3. Duration – persistent, not transient4. Behaviour – impairs coping:
results in disabling behavioural strategies – avoidance, withdrawal
Pathologic Anxiety
Physical symptoms:- autonomic arousal – tachycardia, tachypnea, diaphoresis, diarrhoea, light headedness
Affective symptoms:Mild Severeedginess terror, feeling
loss of control, dying
BehaviourAvoidance, or compulsions (“compensatory”)
Cognitions – worry, apprehension, obsessions
Manifestations of anxiety
Essential education
Anxiety disorders arePrevalent , real, serious, treatable
Anxiety disorders are not
Signs of personal weakness
Shared and specific features of AD
Nutt et al. In: Handbook of Anxiety and Fear 2008
Neurophysiology
Cognitive behavioural formulation
Psychodynamic formulation
Etiology
Central noradrenergic system (NE):locus coeruleus (LC)– major source of brain’s adrenergic innervation. E.g. – stimulate LC – get panic attacks; block LC – decrease
Gamma Amino Butyric Acid (GABA) systemEspecially – septohippocampal areas – mediate generalized anxiety, worry, vigilance- BDZ bind to GABA receptors; reduce vigilance
Serotonergic system (5-HT)Modulate above 2 systems – explains efficacy of multiple clinical interventions – SSRIs, SNRIs, GABA agents, CBT
Neurophysiology (prototypic – panic disorder, generalized anxiety disorder)
Psychopharmaology for anxiety disorders is based on those neurotransmitter systems:1) Norepinephrine
TCAs, Prazosin2) GABA
Benzodiazepines, anticonvulsants3) Serotonergic (5-HT) modulation
- SSRIs, SNRIs, TCAs
Implications
Neurobiology of anxietyLimbic cortex
Periaqueductal Gray matter
Brain Stem
Ventral Tegmental Area
Hippocampus
Amygdala
Nucleus accumbens
Orbitofrontal cortex
Neurobiology of anxietyState anxiety
An interruption of one’s emotional state- become restless, agitated, and then may react/overreact to external stimuli- high state anxiety is unpleasant – pts may seek out “adaptive” behaviours to alleviate this.
Trait anxiety“Stable aspect of personality”- may worry all the time, even with “normal stimuli”, then when there’s a real threatening stimuli – may worry even more
Pharmacotherapy
SSRI or
SNRI(8-12 wks)
GAD
Panic Disorder
OCD
PTSD
Social Anxiety disorder
Alternative StrategiesSwitch Drug
- Another SSRI/SNRI- Clomipramine
- OCD- Panic Disorder
NB NEVER COMBINE SSRI/SNRI with MAOI SSRI + MAOI = DOA(Serotonin Syndrome)
Augment:- Clonazepam- Buspirone (OCD)- Gabapentin
- Panic Disorder- Social phobia- PTSD- Pain
- Atypical Antipsychotic
- GAD, OCD, PTSD
MedicationsSSRIs
- Fluoxetine (Prozac)- Paroxetine (Paxil)- Sertraline (Zoloft)- Fluvoxamine (Luvox)- Citalopram (Celexa)- Escitalopram (Cipralex)
SNRIs- Venlafaxine (Effexor)- Desvenlafaxine (Pristiq)- Cymbalta (Duloxetine)
-PainNDRI
- Bupropion (Wellbutrin, Zyban) (Anxiety worse)
NRI- Atomexetine (Strattera)
- Indicated for ADHD
Focus on information processing and behavioural reactions
Faulty cognitions-e.g. Overprediction of likelihood/degree of catastrophe
Attempts to neutralize anxiety – e.g. With avoidance, compulsive behaviour, paradoxically “lock in” or reinforce anxiety►chronic arousal and anticipatory anxiety
Cognitive Behavioural
Cognitive-behavioural model of anxiety
Trigger
Perception of Danger
Increased Anxiety
- Escape- Avoidance- Safety behaviours
Reinforc
ement
Reduced Anxiety
Cognitive restructuring
Exposure therapy
Reinforcement
Beliefs & Assumptions
Automatic thoughts/Feelings:I am foolish, I am incompetent, I am not loveable
Behaviour: RUN!
Reinforcement: I have not dated; good people don’t like me; I am foolish, I am incompetent, I am not loveable
Single person sees attractive person
Automatic thoughts/Feelings: that person is attractive, I am a good person. Maybe we can be a good match. Let’s find out
Behaviour: Initiate conversation***
Reinforcement: Attractive person seemed to enjoy talking to me. Maybe I have something to offer in a relationship
Cognitive Behavioural Therapy (CBT) is based on these notions
Replace anxiogenic thoughts and behaviours with positive ones.
Implications
Anxiety Thought
• World is dangerous• I am not competent• I can not cope
Coping Thought
• World is safe• I am competent• I can cope
World viewSelf View
Anxiety = threat to the ego; signals are elicited because current events have similarities (symbolic or actual) to threatening developmental experiences (traumatic anxiety)
Object relations theorists emphasize the use of internalized objects to maintain affective stability under stress
Psychodynamic/Developmental
Anxiety Disorders in DSM-IV Panic Disorder without AgoraphobiaPanic Disorder with AgoraphobiaAgoraphobia without history of Panic DisorderSpecific PhobiaSocial PhobiaObsessive-Compulsive DisorderAcute Stress DisorderPosttraumatic Stress DisorderGeneralized Anxiety DisorderAnxiety Disorder Due to General Medical
Condition or Substance-Induced Anxiety Disorder
Anxiety Disorder NOS
Pooled prevalence rates for AD
Somers et al. Can J Psychiatry 2006
9282 pts – english speaking12 month prevalence of numerous psychiatric
disordersAny psychiatric disorder 26.2%Any anxiety disorder 18.1%
National Comorbidity Survey – Replication study
National Comorbidity Study- R
Specific phobia (8.7%)
Social phobia (6.8%)
PTSD (3.5%)
GAD (3.1%)
Panic (2.7%)
OCD (1%)
5
10
Per
cent
age
(%)
Kessler et al. Arch Gen Psychiatry, 2005
Specific PhobiaPersistent and irrational fear of certain
objects or situationsExposure provokes anxiety/panic
responseRecognized as excessive or unreasonablePhobic object/situation avoided or
endured with intense anxiety or distressSignificant interference or marked
distress Types: animals/insects, natural environment,
blood/injury, situational, other
Most common anxiety disorderMarked and persistent fear of clearly
discernible circumscribed objects or situationsExposure almost invariably provokes anxietyFear is recognized as excessive or
unreasonable (though children may not)Phobic stimulus is avoided, or tolerated with
dreadAvoidance/fear leads to significant distress or
interference with social/occ functioningIn children – should persist >6 m
Specific Phobia
Biopsychosocial- Bio- Medications – generally not helpful.
BDZs – may provide some temporary relief (e.g. For flying etc.)
Psychosocial- Exposure therapy – has shown the most benefit
Novel methods - internet based- virtual reality
Treatment
Social Phobia Social Anxiety Disorder
Fear of social or performance situations due to anticipated scrutiny, humiliation or embarrassment
Exposure provokes anxiety/panic Considered excessive or unreasonable Situations avoided or endured with
anxiety Significant interference or suffering Duration > 6 months if age < 18
Generalized or circumscribed
Epidemiology:- 6.8% of the population- Onset - by age 11, 50% have symptoms;
- by age 20, 80% have symptoms- I.E.- CHILDHOOD ONSET
- Children – may refuse to go to school;- Associated with early drop out from
school- Selective mutism – highly likely
becomes social anxiety disorder (severe variant)
Social Phobia
Etiology-Familial, with recurrence risk ratio 2<x<6
i.e. Moderate heritability (chromosome 16 implicated –NE
transporter)Consequences:
- Reduced work productivity- Financial costs- Reduced quality of life
Despite these issues – only half seek treatment, and usually after 15-20 years of suffering
Social Phobia
ALCOHOL /SUBSTANCE ABUSE/DEPENDENCE- Strongly consider underlying social phobia in pts with a history of alcohol abuse/dependence» ¼ of pts may have comorbid abuse
Parkinsons pts – may frequently develop social anxiety – suggesting striatal involvement
Social Phobia - comorbidities
Biopsychosocial approachBio –
Social Phobia - Treatment
SSRIs* SNRIs* RIMAs+MAOIs
AntiCon BDZs
Escitalopram Venlafaxine Moclobemide Gabapentin Clonazepam
Fluvoxamine Phenelzine Pregabalin Alprazolam
Sertraline Divalproex Bromazepam
Paroxetine Topiramate
Citalopram
Fluoxetine1st line: SSRI, SNRI2nd line: BDZ, AntiCon, MAOIs
Other alternatives with evidence of benefitAntidepressants AntipsychoticsBupropion (NDRI) OlanzapineMirtazapine (NaSSa) RisperidoneClomipramine (TCA) Quetiapine
Aripiprazole
Social Phobia
CBT - 12-15 sessions – lasting 50-90 minutes(individual or group therapy)
Correcting distorted cognitions – e.g. Everyone laughing at me – come up with alternative explanations
Exposure therapy – may be integrated in CBT- e.g. Returning item, going to crowded mall
Social skills training- making small talk, looking at tone, posture, active listening, assertiveness
Psychosocial treatments
Epidemiology- 3.1% of the population affected (F:M = 2:1)- Onset
(median US age=31 yrs, but often childhood)
- 25% have onset by 20 yrs old- 50% have onset b/w 20-47 yrs old
- Children- may be “overanxious disorder of
childhood”- >90% comorbidity
Generalized Anxiety Disorder (GAD)
Kessler RC et al. Arch Gen Psychiatry, 2005
Elderly – - may be associated with social isolation, trauma, migration, illness in spouse, bereavement- left untreated – may be associated with medical/psychiatric complications
- Cardio/cerebrovascular disease- COPD- Malnutrition- Depression- Dementia- Alcohol abuse
GAD in elderly (most common anxiety disorder in elderly)
Weisberg R.B. J Clin Psychiatry, 2009
Etiology- Multiple neurotransmitters likely involved
- 5-HT, NE, CCK- Genetic factors likely involved
- Some twin studies – show 50% concordance rate in monozygotic twins, and 15% in dizygotic twins
- Behavioural, psychosocial factors involved
GAD
GAD Clinical FeaturesExcessive, wide-spread and uncontrollable
anxiety and worry ( 6 months)Symptoms of tension and exhaustion
(≥3/6) restlessness, muscle tension, tiredness, irritability,
insomnia, difficulty concentrating(SICKEM – sleep, irritability, conc, keyed up/restless, energy, muscle tension)
NB – children only need ≥1
Worry not confined to another Axis I disorder
Significant distress or impairmentNot due to the effects of substance of GMC
Often – do not present with anxiety initially - May be (somatic)
PainFatigueSleep disturbancesPoor concentrationDepression
- Frequently associated with disabilities in work, education, and/or social interactions
Comorbidities common (>90%) – mood disorders, anxiety disorders, substance abuse
GAD Clinical features
Biopsychosocial approach- Bio
GAD Treatment
SSRIs* SNRIs* TCAs AntiCon BDZs
Escitalopram* Venlafaxine* Imipramine Pregabalin Lorazepam
Alprazolam
Sertraline* Bromazepam
Paroxetine* Diazepam
Citalopram
1st line: SSRI, SNRI x 8-12 wks2nd line: BDZ, NDRI, Buspar, Pregabalin, TCA
Other alternatives with evidence of benefitAntidepressants AntipsychoticsBupropion (NDRI) OlanzapineMirtazapine (NaSSa) Risperidone
OtherBuspirone (Buspar)
With discontinuation of treatment- 20-40% relapse within 6-12 m, suggesting long term treatment is necessary
GAD Treatment
CBT – most evidence for efficacyEfficacy is comparable to pharmacologic
therapy, but may have higher remission ratesOther therapies that may be effective:
- Short term psychodynamic therapy- Interpersonal therapy
Psychosocial Treatment
Panic disorder +/- AgoraphobiaPanic attacks (PA)
Recurrent and unexpected, acute, time-limited symptoms (at least 4/13)
Not caused by substance or GMCNB Panic attack ≠ Panic disorder (yet)
Anticipatory anxiety Concern about additional attacks, their implications
and consequences or change in behaviour 1 month
Agoraphobia Avoidance/distress/anxiety in places or situations
difficult to escape or get help in case of PA
Panic attacks – may come from a dysfunction of the fear circuitry
Amygdala – central involvement- Consists of several distinct nuclei in the brain
Very high comorbidity- 50-60% may have comorbid major depressive disorder
Etiology
YohimbineLactateCO2CaffeineIsoproterenol5HT agonists (fenfluramine, m-CPP)Choleocystokinin (CCK-4, CCK-5)Stimulants – nicotine, amphetamines
Substances that elicit panic
Biopsychosocial approach- Bio
Panic Disorder Treatment
SSRIs* SNRIs* TCAs AntiCon BDZs
Escitalopram Venlafaxine Imipramine Gabapentin Lorazepam
Fluoxetine Clomipramine Divalproex Alprazolam
Sertraline
Paroxetine Diazepam
Citalopram Clonazepam
Fluvoxamine
1st line: SSRI, SNRI2nd line: BDZ, NaSSA, TCA3rd line: Anticon, MAOI, Atypical Antipsych, RIMA, pindolol
Other alternatives with evidence of benefitAntidepressants AntipsychoticsBupropion (NDRI) OlanzapineMirtazapine (NaSSa) Risperidone
QuetiapineOther: Pindolol
SSRI Benefits – may be seen within 1 wk;- up to 6-8 wks
Continued benefits may be seen after 12 m Treatment time of 8 -12 m is suggested, to
prevent relapse risk.
Panic Disorder Treatment
CBT – most evidence for efficacyEfficacy is comparable to pharmacologic
therapy, but may have higher remission ratesOther therapies that may be effective:
(BUT – INSUFFICIENT evidence to recommend)- Psychodynamic therapy- Eye Movement Desensitization and Reprocessing (EMDR)
Psychosocial Treatment
Epidemiology- 1% of population (F:M= 3:2)- Onset – median age 19 yrs old, though can be childhood onset (NB – in childhood, F:M= 1:2)- Children
Obsessive Compulsive Disorder (OCD)
Etiology:- Dysregulation of 5-HT*- Genetics – significant
35% of 1st degree relatives of OCD also have OCD- Neuroimaging studies
- show increased metabolism of frontal lobes, caudate and cingulum
- Behavioural, psychosocial factors involved
Obsessive Compulsive Disorder (OCD)
Obsessions +/- compulsionsObsessions
recurrent, persistent thoughts, urges or images experienced as intrusive and anxiety-provoking, distinct from excessive worry, attempted to be suppressed, ignored or neutralizedcontamination, harm/aggression, somatic, religious, sexual
Compulsions repetitive, excessive behaviours or mental acts and
rituals aimed to prevent or decrease anxiety/distresscleaning, checking, counting, repeating, arranging, hoarding
Obsessions or compulsions are time consuming (>1 hr/day) or cause clinically significant distress
At some point – obsessions/compulsions are recognized as excessive or unreasonable(may not occur in childhood)
Not due to medical condition/substance
OCD
Obsessions – are distressing – e.g. Repeated thoughts about contamination
Usual response – compulsion – a behaviour aimed at reducing the anxiety associated with obsession – e.g. wash hands – temporary relief from anxiety of obsession, but then obsession returns.
Egodystonic: i.e. “alien”, not within his/her control BUT – recognized as product of the mind (i.e. Not thought insertion)
OCD
Children - clinical features:- Most frequent compulsion children
- Handwashing (75%)- Checking- Sorting
May not be egodystonic – often brought by parents
Small subset (<5%) – ass with Gp A β-hemolytic streptococcal infection (scarlet fever, “strep throat”) abrupt onset, with motor abnormalities = PANDAS (Paediatric Autoimmune Neuropsychiatric Disorder Ass with Streptococcal infection)
OCD
Elderly onset – more concerns about morality and washing rituals.
Comorbid issues with OCD“Depressing BODY TAASTE”:- Depressive disorder- Body dysmorphic disorder- Trichotillomania and other impulse control d/o- Anxiety Disorders- Autism- Schizophrenia- Tourette’s/Tic disorders- Eating Disorders e.g. Anorexia nervosa
OCD
Biopsychosocial (NB lowest response rate to placebo among anxiety disorders)
- Bio
OCD treatment
SSRIs* SNRIs* TCAs AntiCon AntiPsych
Escitalopram Venlafaxine Gabapentin Risperidone
Fluoxetine Clomipramine Topiramate Olanzapine
Sertraline IV Clomipramine
Quetiapine
Paroxetine Haloperidol
Citalopram
Fluvoxamine
1st line: SSRI2nd line: Clomipramine, SNRI, NaSSA, Risperidone3rd line: Something else....antipsych, anticon, MAOI
Dosages of meds e.g. SSRIs may need to be higher
Response may take 6 wks or longerMost recommendations – suggest staying on
treatment for 1-2 yrs (reduce relapse risk)
Pharmacology issues
Neurosurgical options- deep brain stimulation - anterior cingulotomy- anterior capsulotomy,- subcaudate tractotomy- limbic leucotomy
Indicated for severe OCD, refractory to therapy/medications
40-60% of refractory pts may benefit
Another option...
CBT with Exposure Response Prevention (ERP)- the most evidence for efficacy for treatment
Individual may be better than group (individualization of treatment)
Psychosocial treatment
Anxiety in 5 4 slides….
Epidemiology – genetics, environment♀>♂, usually 2:1. OCD the exception (1:1)
Look at Trigger:1) Constant- GAD (6 months)2) Groups of People – Social Phobia (6 months)
3) Parents – Separation4) Objects/animals – phobia*** commonest5) Trauma – PTSD (>1 month)6) “Out of the Blue” – Panic (>1 month)7) Contamination, “bad things happening”– OCD
NB: Egodystonic Streptococcus possibility(PANDAs)
Anxiety Disorders
*Childhood onset
*
Comorbidity: MAJOR DEPRESSIVE DISORDER (all)- Social Phobia – Alcohol dependence- OCD – Depressing BODY TAASTE
Neurotransmitters involved:5-HT (esp OCD) NE GABA
Structures: Amygdala
Anxiety Disorders
Amygdala
Bio (Pharmacotherapy)
SSRI or
SNRIHigher doses(8-12 wks);
(BDZ short termexcept OCD)
GAD
Panic Disorder
OCD
PTSD
Social Anxiety disorder
OCD – Can also do neurosurgery
Psychosocial
CBT(ERP with OCD)
GAD
Panic Disorder
OCD
PTSD
Social Anxiety disorder
EMDR – Used with PTSD
Anxiety is common – we all experience thisPathological anxiety can also be common, and
is not a sign of personal weakness.Important, but sometimes difficult to
recognize. There are significant biological underpinnings
to anxiety disorders.Psychological approaches are very effective.Treatment can be very effective, but should be
tailored to individual patients.Use BIOPSYCHOSOCIAL approach.
Summary
Questions?