Presentation on theme: "Anxiety Disorders Alan L. Podawiltz, MS, DO Associate Professor of Psychiatry & Behavioral Sciences (UNTHSC) The University of North Texas Health Science."— Presentation transcript:
Anxiety Disorders Alan L. Podawiltz, MS, DO Associate Professor of Psychiatry & Behavioral Sciences (UNTHSC) The University of North Texas Health Science Center John Peter Smith Health Network
What is anxiety? Universal emotion State of heightened apprehension Associated symptoms Excessive worry Avoidant of anxiety provoking stimuli Anxiety results from unknown internal stimuli; excessive when compared to the existing external stimulus Fear is a sense of dread and foreboding in response to external threat. (technically not an anxiety disorder)
Anxiety Disorders Core symptoms in Anxiety Disorders is the excessive experience of anxiety GAD - no specific triggers > uncontrollable worry PD – episodic bouts of anxiety SAD – social, performance SP – situation or objects OCD – intrusive ideas > ritualistic behaviors PTSD – pattern of cognition invoking the emotional memory of the trauma
Manifestations of Anxiety Physical symptoms: autonomic arousal such as tachycardia, tachypnea, diarrhea, diaphoresis, lightheadedness Affective symptoms: feelings of being edgy, terror “going to die or lose control” Cognitive symptoms: worry, apprehension, obsessions, thought about body and emotional damage Behavior symptoms: avoidance, withdrawal, compulsions and rituals
Anxiety Disorders (Etiology) A. Neurophysiology 1.Central noradrenergic systems- locus coeruleus major source of adrenergic innervation, stimulation – panic symptoms, blockade- relief of symptoms 2.GABA – limbic system mediate general anxiety, worry and vigilance. 3.Serotoninergic & neuropeptides – modulates GABA and noradrenergic systems
Anxiety Disorders (Etiology) B. Cognitive Behavioral Formulation 1.Role of thoughts and beliefs in activating anxiety 2.Avoidance and escape responses maintain fear and dysfunctional thinking patterns. C. Psychodynamic Formulation Signal of threat to the ego, current events have similarities to threatening developmental events.
Anxiety Disorders -Public Health Aspects Common group of disorders One in four reports a lifetime history of one (or more) anxiety disorders 30 million have suffered anxiety disorders 6% men, 13% women within the last 6 months Often seen in primary care settings Chronic and complicated with depression and substance abuse
Prevalence of Anxiety Disorders in US Population Disorder Lifetime Prevalence (%) 12 months (%) Any Anxiety Disorder 24.917.2 Panic Disorder3.52.3 Agoraphobia5.32.8 Social Phobia13.37.9 Simple Phobia11.38.8 Generalized Anxiety Disorder 5.13.1
Post Traumatic Disorder (Diagnosis) A. Exposure to a traumatic event in which both of the following were present: Experienced, witnessed or confronted with an event that involved threat to life, physical integrity to self or others or serious injury. Response was intense fear, helplessness and horror.
Post Traumatic Disorder (Diagnosis) B. The traumatic event is persistently experienced in one or more of the following ways: (Re-experiencing) Recurrent and intrusive recollections of the event Acting or feeling as if the event were recurring Intense psychological distress at exposure to internal or external cues symbolizing or resembling the event. Physiological reactivity on exposure to the internal or external cues symbolizing or resembling the event.
Post Traumatic Disorder (Diagnosis) C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness as indicated by 3 or more of the following: (Numbing) Efforts to avoid thoughts, feelings or conversation (associated with the trauma) Efforts to avoid activities, places or people arousing recollections of the trauma Inability to recall important aspect of the trauma Markedly diminished interest or participation in significant activities. Feeling of detachment or estrangement from others Restricted range of affect Sense of a foreshortened future
Post Traumatic Disorder (Diagnosis) D. Persistent symptoms of increased arousal as indicated by two (or more) of the following: (i.e. hyperarousal) Difficulty falling or staying asleep Irritability or outbursts of anger Difficulty concentrating Hypervigilance Exaggerated startle response
Post Traumatic Disorder (Diagnosis) Duration of symptoms B,C,D is more than one month The disturbance causes clinically significant distress and functional impairment. Acute: duration less than 3 months Chronic: duration 3 months or more With delayed onset: onset of symptoms at least 6 weeks after the stressors
Post Traumatic Stress Disorder (Etiology) Trauma/Stressor (PTSD, Acute Stress Disorder, Adjustment Disorder) The subjective experience of the stress is more significant factor than objective severity in development of the disorder
Post Traumatic Stress Disorder (Etiology) Childhood trauma, personality disorders, poor support system, recent life stressors, excessive alcohol use and perceived external locus of control as opposed to internal are all predisposing factors that increase vulnerability. Neurotransmitter imbalance, increase ANS response Partial ability to cognitively cope with the event
Post Traumatic Stress Disorder (Etiology) Behavioral model: Phase 1: unconditioned stimulus (trauma) is paired with the conditioned stimulus (physical, mental reminders of the trauma). Phase 2: Instrumental learning: pattern of avoidance of both stimulus Psychoanalytic model: reactivation of previously quiescent, unresolved psychological conflict.
Post Traumatic Stress Disorder (Epidemiology) Prevalence: Lifetime general population 1-3 % High risk group: 5-75 % Vietnam veterans: 30% Age of onset: Any age, usually young adult Common types of trauma: Men - combat Women - rape Both - accidents, assault, natural disasters
Panic Disorder - (Diagnosis) Recurrent, spontaneous, primary panic attacks (4 out 13 panic symptoms) At least one of the attacks has been followed by 1 mo. or more of one or more: Persistent concern about having an attacks Worries about implications of the attack Behavioral changes related to the attacks (avoidance phobic symptoms)
Eponyms of Post Traumatic Stress Disorder In Various U.S. Wars War Disorder Civil War Irritable Heart WW I Effort Syndrome WW II Combat Stress Reaction Vietnam War Post Traumatic Stress Disorder Gulf War Gulf War Syndrome ? ____ _______ (fatigue, shortness of breath, palpitations, headache, muscle and joint pain, dizziness, disturbed sleep, difficulty concentrating and forgetfulness)
Most Upsetting Trauma in Primary Care Cases of PTSD Sexual Assault : 23% Accident: 19% Witness Death Injury: 15% Nonsexual violence:15% Natural disaster: 9%
Post Traumatic Stress Disorder (Treatment) Pharmacotherapy: at least one year. Effective in depression, anxiety and hyperarousal: TCAs, MAOIs; AEDs, clonidine, beta blockers
Post Traumatic Stress Disorder (Treatment) Psychotherapy: time limited to prevent dependency and chronicity Acute: crises intervention, support, education, development of coping skills Chronic: exposure - imaginal or in vivo (lasting effect) stress mgt – relaxation and CBT (rapid effect) Group therapy: shared experience
Obsessive Compulsive Disorder (Diagnosis) Obsessions: 1.Recurrent, persistent, intrusive or inappropriate thoughts, images or impulses 2.Not simply excessive worries about real-life problems 3.Attempts to ignore or suppress thoughts, impulses or images 4.Individual recognizes that the thoughts, impulses, or images are a product of his or her mind Distress either obsessions or compulsions:
Obsessive Compulsive Disorder (Diagnosis) Compulsions: 1.Repetitive behaviors that a person feels driven to preform 2.Behaviors or mental acts are aimed at preventing dreaded event or reducing anxiety
Obsessive Compulsive Disorder (Diagnosis) Recognition that the obsessions and compulsions are excessive or unreasonable The obsessions or compulsions cause marked distress and are time consuming (more than 1 hr/day) Functional impairment secondary to the condition
Obsessive Compulsive Disorder (Course and Prognosis) Onset may be sudden or following a stressful life events Often kept secret for years 1/3 have significant improvement, 1/3 moderate improvement, & 1/3 have no improvement Good prognosis for sudden onset and good ability to resist compulsions (with insight)
Obsessive Compulsive Disorder (Treatment) Pharmacotherapy: SSRIs are of choice, clomipramine (a serotonergic TCA), atypical antipsychotics Behavior therapy: exposure & response prevention (ERP), assertiveness training Surgery: cingulotomy, subcaudate tractotomy, stereotactic limbic leukotomy Treat usual comorbid disorders: Tourette’s disorder, depression, psychosis, eating disorders and body dysmorphic disorder.
Obsessive Compulsive Disorder (Clinical Pearls) Recognition is usually difficult, collateral information needed Partial treatment response common Longer trial period and higher doses of SSRIs, clomipramine Combination therapy considered optimal for long term treatment (i.e. CBT* and antidepressant) *CBT - Cognitive Behavioral Therapy
Symptoms of Panic Attacks 1.Palpitations 2.Sweating 3.Trembling or shaking 4.Shortness of breath 5.Feeling of choking 6.Chest pain or discomfort 7.Nausea 8.Dizziness or lightheadedness 9. Derealization/ Depersonalization 10. Fear of losing control or going crazy 11. Fear of dying 12. Paresthesias 13. Chills or hot flushes
Panic Disorder (Epidemiology) Life time prevalence about 3.5% More frequent in women Onset between 20 and 30 years old; unusual after 40 Life events 6 months prior often associated with onset In 78% of initial attacks no trigger occurs
Agoraphobia (Diagnosis) Fear in places or situations where escape might be difficult, help may not be available, being trapped or embarrassed Fear of being alone and often require companion when leaving the house Typical situations that elicit fear are public transportation, crowds, elevators Majority are accompanied by panic disorders
Agoraphobia (Epidemiology) Lifetime prevalence - 5.3 %; 12 month prevalence - 2.8 % Prevalence usually difficult to ascertain, patient usually don’t seek help Psychiatric settings, about 75 % of agoraphobics have panic disorder
Agoraphobia (Treatment) Gradual exposure is most effective Pharmacotherapy as in Panic Disorder
Panic Disorder (Etiology) Catecholamine theory: excessive beta adrenergic discharge Increase norepinephrine in locus coeruleus Decreased inhibition due to abnormal GABA receptors Can be induced by administration of sodium lactate
Panic Disorder (Etiology) Single locus autosomal dominant with incomplete penetrance Psychoanalytic: anxiety secondary to repressed conflict Behavior theory: classical conditioning Cognitive behavior theory: dysfunctional thoughts → dysfunctional affect
Panic Disorder (Course and Prognosis) Periods of remission and relapse Severity varies Effects on functioning can be significant Significantly increased risk for suicide Prognosis depends on symptom severity and premorbid functioning
Panic Disorder (Treatment Options) Pharmacotherapy: Antidepressants SSRI, SNRI, TCA, MAOIs are effective long term maintenance treatment AEDs gabapentin & pregabalin have mixed results Cognitive behavior therapy Psycho education and support Combination treatment strategies
Clinical Pearls Panic DO patients aggressively seek help In agoraphobia the key question is: What are you afraid of? Activation syndrome with antidepressant treatment: Educate, start low, go slow Better outcome for combination treatment (medication and psychotherapy) Treat comorbid disorders of depression and substance abuse
Social Phobia (Diagnosis) Marked persistent fear of one or more social or performance situations (eating, writing, using public restrooms) in which the person is exposed to unfamiliar people or possible scrutiny. Exposure provokes anxiety in the form of situational bound panic attacks Recognizes that the fear is unreasonable or excessive Feared situations are avoided or endured with distress
Social Phobia (Epidemiology) Phobias are the most prevalent psychiatric disorders with a lifetime prevalence of 13.3 % & a 6 months prevalence of 7.9 % Frequent in women, lower education, never married, lives with parents Median age of onset 16 y/o; rare onset after 25 Association with substance abuse is low
Social Phobia (Etiology) Genetic theory: character traits of inhibition, shyness, fear of social criticism, social introversion Psychoanalytic: less caring, over protective parenting style Behavior theory: skill deficit, cognitive inhibition, conditioned anxiety models
Social Phobia (Course and Prognosis) Chronic and unremitting Prognosis depends upon the extent of functional impairment and presence of co morbid disorders
Social Phobia (Treatment) Pharmacotherapy: antidepressants such as SSRIs, SNRIs, MAOIs; also benzodiazepines & beta blockers (for performance subtype) Behavior therapy: exposure, cognitive restructuring, social skills training, group therapy Combination therapy: to sustain remission
Specific Phobia (Diagnosis) Circumscribed fear of a focal object or situation such as flying, heights, animals, blood, injection Exposure to phobic stimulus provokes immediate anxiety response Recognizes that fear is excessive, unreasonable Phobic situation avoided or endured with distress
Specific Phobia (Epidemiology) Prevalence lifetime of 11.3% and a 12 months prevalence of 8.8% Frequent in women, average age of onset 25 years old Blood injury phobia begins in adolescence Childhood onset phobias often remit spontaneously
Specific Phobia (Etiology) Genetic theory: familial transmission and high concordance rate in twin Behavior theory: classical conditioning with object and situation paired with fear Specific experience or modelling Vasovagal reflex is inherited in blood injury phobias
Specific Phobia (Treatment) Behavior therapy with graded exposure hierarchy of feared stimuli Relaxation techniques are helpful PRN beta blockers PRN benzodiazepines Self medication with alcohol is unfortunately quite common
Acute Stress Disorder (Diagnosis) A new disorder added to DSM IV Involves exposure to a traumatic event with both of the following: Experienced, witnessed, or confronted with an event that involved threat to life, serious injury, threat to physical integrity to self or others. Response was intense fear, helplessness and horror
Acute Stress Disorder (Diagnosis) Three or more dissociative symptoms during or after the events: Numbing, detachment, absence of emotion Reduction in awareness of the surroundings Derealization Depersonalization Dissociative amnesia
Acute Stress Disorder (Diagnosis) Persistent re-experiencing of the event: including images, thoughts, dreams, illusions, flashbacks, sense of reliving the experience. Marked avoidance of stimuli that arouse the recollections of the trauma Functional impairment in daily activities Marked symptoms of anxiety or increased arousal.
Acute Stress Disorder (Diagnosis [cont] ) Last for a minimum of two days & a maximum of four weeks and occurs within four weeks of the traumatic event Not due to the direct physiological effects of a substance or a general medical condition
Acute Stress Disorder (Treatment) Symptoms may serve as adaptation to function in the immediate aftermath Brief prevention program within 2 wks of an assault : education, relaxation, exposure, cognitive restructuring decrease likelihood of developing PTSD Critical Incident Stress Debriefing: civilian trauma Beta blockers may be helpful; benzodiazepines may interfere with learning process
Generalized Anxiety Disorder (Diagnosis) A.Excessive anxiety and worry occurring more days than not for at least 6 months (about number of events or activities) B.Difficult to control the worry C.Associated with 3 or more of the following six symptoms: - restlessness - irritability - being easily fatigued - muscle tension - difficulty concentrating - sleep disturbance
Generalized Anxiety Disorder (Diagnosis) Biological theory: GABA deficiency, reduced sensitivity of alpha 2 receptors, abnormal regulation of the serotonin system, lower metabolic rate in basal ganglia and white matter. Psychosocial factors: cognitive distortions, focus on negative details and inaccurate perception of ability to cope. Psychoanalytic: unresolved conflicts - fear of fusion - castration anxiety - separation anxiety - super ego anxiety
Generalized Anxiety Disorder (Epidemiology) Lifetime prevalence: 5.1 % 12 months prevalence: 3.1 % 2:1 women to men Commonly coexist with other psychiatric and medical diagnosis Usually in the 20’s and 30’s 1/3 seek help from nonpsychiatric providers
Generalized Anxiety Disorder Course and Prognosis Difficult to predict Several negative life events associated with GAD Chronic condition 25% will have panic disorder; 50% major depression and / or substance abuse
Generalized Anxiety Disorder (Treatment) Combination therapy (SSRI and psychotherapy) Pharmacotherapy must be carefully initiated: SSRI, TCA, antihistamines, Anti-seizure medications, beta blockers, buspirone, clonidine, benzodiazepine, Benzodiazepine: defined target symptoms and length of treatment: 2-6 weeks then taper to discontinue. Indefinite Tx: common mistake because of sedation, confusion, tolerance and withdrawal Psychotherapy: CBT, insight oriented, psychodynamic: increase capacity to tolerate anxiety
Mood, Emotion, Cognitive function Motivation Sex Appetite Aggression Anxiety Irritability Energy Interest Impulsivity Drive Norepinephrine Serotonin Dopamine Major Neurotransmitters
J Clin Psychiatry. 2005;66 Suppl 2:9-13. The effects of benzodiazepines on cognition. Stewart SA. Author information Massachusetts General Hospital, Boston, MA 02478, USA. firstname.lastname@example.org Initially thought to be virtually free of negative effects withdrawal, and negative side effects. Among the most controversial of these side effects are cognitive effects. Long-term treatment with benzodiazepines impairment in several cognitive domains visuospatial ability, speed of processing, and verbal learning. Meta-analyses of peer-reviewed studies found that cognitive dysfunction did in fact occur in patients treated long term with benzodiazepines, and although cognitive dysfunction improved after benzodiazepines were withdrawn, patients did not return to levels of functioning that matched benzodiazepine-free controls. Such findings suggest that patients should be advised of potential cognitive effects when treated long term with benzodiazepines, although they should also be informed that the impact of such effects may be insignificant in the daily functioning of most patients.
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